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THE FUNDUS OCULI.

NUNQUAM ALIUD NATURA, ALIUD SAPIENTIA DICIT.

THE

FUNDUS OCULI

WITH AN

OPHTHALMOSCOPIC ATLAS

ILLUSTRATING ITS PHYSIOLOGICAL & PATHOLOGICAL

CONDITIONS.

W. ADAMS FROST, F.R.C.S.,

OPHTHALMIC SURGEON, ST. GEORGE’S HOSPITAL *, SURGEON TO THE ROYAL
WESTMINSTER OPHTHALMIC HOSPITAL.

EDINBURGH AND LONDON :

YOUNG J. PENTLAND.

1 896.

EDINBURGH I PRINTED FOR YOUNG J. PENTLAND, II TEVIOT PLACE, AND 38 WEST
SMITHFIELD, LONDON, E.C., BY SCOTT AND FERGUSON AND JUJRNESS AND COMPANY.

| ROYAL col:

PREFACE.

The ophthalmoscope is no longer the instrument of the few.
Nearly all students in our medical schools learn its use. That
most of them, when in practice, neglect to employ it as a means
of diagnosis is, I believe, largely due to the want of a key to

interpret what it reveals. One object of this work is to supply

this deficiency.

The physician, using the word in its more special sense, finds
the ophthalmoscope as ‘essential in some cases as the stethoscope
in others. He may often, however, be left in doubt or led astray

by want of familiarity with conditions of the fundus which have

no direct bearing upon the diagnosis. It is chiefly with the
view of meeting this difficulty that “ physiological variations”
have been so fully dealt with in the following pages.

To professed ophthalmologists I offer no apology for a work
that can contain little that is new to them. For I presume that
their wants are similar to my own. I have often felt the need,
for teaching purposes, of a series of drawings of the fundus, more
varied and more modern than those which we possess.

All honour to those who first depicted for others appearances
which they had themselves been among the earliest to repognise.
The Atlases which they produced are, and must ever remain,
monuments of patient labour and artistic skill. But these older

PREFACE.

viii

works have become scarce, and our knowledge of ophthalmoscopic
appearances has advanced since they were published.

It seems to me, therefore, that the time has come when we
may, with advantage, take stock of our knowledge. If we agree
as to facts, we shall not dispute much over theories. If we can
agree as to what may be considered known, we shall advance
with greater safety into the great unknown.

In the body of the work I have endeavoured to summarise
our knowledge of such conditions of the fundus as are likely to
be met with in the ophthalmic clinique of a large hospital.

The figures in the coloured plates have, with few exceptions,
been drawn from cases occurring in my own practice, and I am
greatly indebted to the artist, Mr. A. W. Head, for the care
and skill with which he has executed the drawings.

In conclusion, I beg to thank numerous friends for much
valuable advice, particularly Dr. Penrose, for the revision of those
parts of the book which deal with general medicine, and Mr.
Sydney Stephenson, for assisting me in correcting the proof sheets.

17 Queen Anne Street,

London, W., May 1896.

CONTENTS.

PAGE

INTRODUCTION, ......... 1

PART I.— PHYSIOLOGICAL VARIATIONS.

CHAPTER I.

THE NORMAL FUNDUS, ........ 9

Sclerotic — Choroid — Retina.

CHAPTER II.

THE OPTIC DISC, ......... 28

Optic Nerve — Sheaths of Optic Nerve — Blood Vessels of Optic Nerve — Terms
“Disc” and “Papilla” — Division into three Zones — Central Zone — Porus
Opticus — Physiological Cup — Intermediate Zone — Variations in Colour — Varia-
tions in Level — Margin — Distribution of Nerve Fibres — Reflex from Nerve
Fibres — Hypermetropic Disc — Connective Tissue Ring — Scleral Ring — Pigment
Ring — Oval Shape.

CHAPTER III.

THE RETINAL VESSELS, ........ 47

Ophthalmoscopic Appearance of Arteries and Veins — Central Light-Streak —
Distribution on the Retina — Cilio-Retinal Vessels — -Unusual Tortuosity —
Bifurcating Veins — Projecting Loops — Persistent Hyaloid Artery — Pulsation
in Retinal Vessels.

CHAPTER IV.

THE MACULA LUTEA, ........ 62

Definition — Anatomy — Ophthalmoscopic Appearance — Radiating Striie — Reflex
Ring — Foveal Reflex — Blood Vessels of Macula — Gunn’s Dots.

CONTENTS.

CHAPTER V.

PAGE

DEVELOPMENTAL IRREGULARITIES, ...... 68

Coloboma of Choroid — Opaque Nerve Fibres — Congenital Crescent of the Disc —

Coloboma of the Disc.

PART II.— PATHOLOGICAL CONDITIONS.

CHAPTER VI.

AFFECTIONS OF THE CHOROID, ....... 87

Choroiditis — Classification — Disseminated Choroiditis— Stage of Exudation — •

Atrophic Stage — Stage of Complications — Choroiditis of Macular Region —

Diffuse Choroiditis and Choroido-Retinitis — Choroido-Retinal Sclerosis — Causes
of Choroiditis — Rupture of Choroid.

CHAPTER VII.

OPTIC NEURITIS OR PAPILLITIS, . . . . . .114

Anatomical Considerations — Definition of Terms — Physiological Variations of
the Disc — Symptoms of Papillitis — ■“ Choked Disc ” and “ Descending
Neuritis” — Causes of Papillitis — Papillitis from Orbital Causes — Papillitis
from Intracranial Orbital Causes — Papillitis from General Orbital Causes—

Results of Papillitis.

CHAPTER VIII.

NEURO-RETINITIS AND RETINITIS, . . . . . .133

Symptoms — Subsidence — Degeneration — Stellate Figure at the Macula —
Albuminuric Retinitis — Diabetic Retinitis — Leucocythaemic Retinitis— Retinitis
Circinata — Plastic Retinitis and Cicatricial Changes.

CHAPTER IX.

OPTIC ATROPHY, ......... 147

Post-Neuritic Atrophy — Simple Atrophy — Hereditary Optic Atrophy — Secondary
Atrophy — Simple Glaucoma.

CHAPTER X.

AFFECTIONS OF THE VASCULAR SYSTEM OF THE RETINA, . . 158

General Considerations — Hyaline Thickening — Sclerosis of Walls — Aneurism —

New Vessels in the Vitreous— Intraocular Haemorrhage — Recurrent Haemorrhage
in Young Men--- Arterial Embolism and Thrombosis — Symptoms — Re-establish-
ment of the Circulation — Thrombosis of the Vena Centralis — Symmetrical
Changes at the Macula in Infants — Leukaemic Retinitis.

CONTENTS.

CHAPTER XI.

PUNCTATE CONDITIONS OF THE FUNDUS, .

Gunn’s Dots — Metallic Dots — Neuritic Dots — Hyaline Excrescences from
Lamina Yitrea — Nettleship’s Dots, associated with Night Blindness — Tay’s
Choroiditis — Colloid Change in Pigment Layer — Hyaline Proliferations on
the Disc.

CHAPTER XII.

PIGMENT CHANGES IN THE RETINA, ......

Retinitis Pigmentosa — Pigment Streaks on the Fundus.

CHAPTER XIII.

DETACHMENT OF THE RETINA, .......

Causes — Ophthalmoscopic Appearance — Commotio Retinae.

PAGE

199

204

213

INDEX, .

221

LIST OF ILLUSTRATION S.

(a.) FIGURES IN THE TEXT.

FIG.

1. Diagram to illustrate the enlargement of the image in direct ophthalmoscopic examination,

2. Horizontal section of eyeball. (Arlt and Efinger), .....

3. Perpendicular section of choroid, .......

4. Choroidal capillaries seen in horizontal plane, ......

5. Diagram of the vessels of the choroid. (Graefe and Saemisch),

6. Pigment epithelium of retina. (Graefe and Saemisch), ....

7. Perpendicular section through human retina, ......

8. Diagrammatic section of retina. (Merkel), ......

9. Section through optic nerve and papilla, .......

10. Diagram of blood vessels of optic nerve and disc. (Graefe and Saemisch),

11. Disc appearing to be oval from astigmatism, ......

12. Oval disc, ..........

13. Cilio-retinal vessels of large size, .......

14. Tortuosity of arteries and veins, ........

15. Cork-screw twist of retinal vein, .......

16. Projecting loops in retinal vessels, .......

17. Do. do. (Randall), ......

18. Bifurcating vein, .........

19. Abnormalities in retinal veins. (Werner), ......

20. Do. do. (Stephenson), ......

21. Communicating branch between veins, .......

22. Bifurcating vein. (Stephenson), .......

23. Bifurcating retinal veins. (Stephenson), ......

24. Do. (Randall), .......

25. Vessel projecting into vitreous from the disc, ......

26. Remains of hyaloid artery, ........

27. Section of retina in macular region. (I)immer), .....

28. Section through the macula. (Bird and Schafer), .....

29. Entoptic appearance of vessels at macula. (Graefe and Saemisch),

30. Diagram of lamina cribrosa, ........

31. Diagram of hypothetical condition of lamina cribrosa in congenital crescent,

page

16
21
22
29
31

54
54

64
66
78
78

XIV

LIST OF ILLUSTRATIONS.

FIG.

32. Coloboma of optic disc. RE. (Benson), .....

33. Do. do. LE. do. .....

34. Do. do. (Randall), .....

35. Partial defect in disc, ........

36. Hypersemia of the choroid from a recent wound of the eye,

37. Diagram showing the semi-decussation at the chiasma, ....

38. Section through optic nerve and papilla, .....

39. Section through macula. (Bird and Schafer), .....

40. Glaucomatous cup, ........

41. Diagram to explain apparent break in a vein where crossed by an artery,

42. Symmetrical changes at the macula in infants (inverted). RE. Mr. Warren Tay’s case,

43. Do. do. LE. do.

44. Leukiemic retinitis, . . .....

45. Retinal pigment streaks, Mr. Doyne’s case, .....

46. do. Mr. Stephenson’s case, .....

page

115

116
135
156
161
191
191
196
210
211

(b.) FULL-PAGE PLATES.

PLATE

I. Physiological Cupping of Optic Disc.

Fig. 1. Physiological Cup.

,, 2. Do. Connective Tissue Ring.

„ 3. Do. Oval Disc. Striation of Upper and Lower Borders.

II. Retinal Reflex.

Fig. 4. Moderately Dark Fundus. Striation of Disc Margin. Dark Macula.

,, 5. Very Dark Fundus. Retinal Reflex. Oval Disc. Fovea Centralis conspicuous.

,, 6. Dark Fundus. Retinal Striation Limited to Disc-Margin. Disc of rich red

colour.

III. Fundi, showing Choroidal Vessels.

Fig. 7. Light Fundus. Choroidal Vessels with Light Interspaces.

„ 8. Dark Fundus. Choroidal Vessels with Dark Interspaces. Retinal Reflex.

IV. Congenital Crescent of Optic Disc.

Figs. 9 and 10. Congenital Crescents. “Gunn’s Dots.”

V. Variations of Disc Margin.

Fig. 11. Pigment on Disc. Connective Tissue on Disc.

,, 12. Absence of Central Zone of Disc. Peculiar Colour. Connective Tissue Ring.

„ 13. Physiological Cup. Narrow Crescent on Temporal Border.

,, 14. Grey Red Disc. Exaggerated Connective Tissue Ring.

VI. Congenital Crescent of Optic Disc.

Fig. 15. Congenital Crescent.

„ 16 and 17. Congenital Crescents. Large Physiological Cups.

LIST OF ILLUSTRATIONS.

PLATE

VII.

VIII.

IX.

XI.

XII.

XIII.

XIV.

XV.

XVI.

XVII.

XVIII.

Congenital Crescent of Optic Disc.

Figs. 18 and 19. Congenital Crescents. Tortuous Veins.

„ 20 and 21. Congenital “ Mottled ” Crescents.

Congenital Crescent and Coloboma of Disc.

Fig. 22. Congenital Crescent.

„ 23. Do. Above.

„ 24. Congenital Abnormality of Disc (Partial Coloboma).

„ 25. Coloboma of Disc.

Coloboma of Fundus.

Fig. 26. Coloboma of Fundus.

„ 27. Do. do.

Congenital Pigment Dots on Fundus.

Fig. 28. Congenital Pigment Dots.

„ 29. Do. do.

Punctate Conditions of Fundus.

Fig. 30. Physiological Dots in Macular Region. (“ Gunn’s Dots.”)
„ 31. Diffuse Punctated Condition of Retina.

Connective Tissue on Disc and Opaque Nerve Fibres.

Fig. 32. Connective Tissue on Disc.

„ 33. Do. do.

„ 34. Opaque Nerve Fibres.

,, 35. Do. do.

Opaque Nerve Fibres.

Figs. 36 and 37. Opaque Nerve Fibres.

Opaque Nerve Fibres.

Fig. 38. Opaque Nerve Fibres.

„ 39 Do. do.

Choroiditis.

Fig. 40. Choroiditis. Early Stage.

„ 41. Do. Advanced.

Choroiditis.

Fig. 42. Choroiditis. Advanced.

Choroiditis. Advanced.

Fig. 43. Choroiditis. Secondary Pigmentation of the Retina.
Disseminated Choroiditis.

Fig. 44. Disseminated Choroiditis with Conspicuous Pigmentation.

XVI

LIST OF ILLUSTRATIONS.

PLATE

XIX. Pigmentation of Retina Secondary to Choroiditis.

Fig. 45. Pigmentation of Retina from Choroiditis.

XX. Disseminated Choroiditis.

Fig. 46. Disseminated Choroiditis. Stage of Exudation.

„ 47. „ „ Stage of Atrophy.

XXI. Choroiditis. Atrophic Stage.

Fig. 48. Areas of Choroidal Atrophy without Pigmentation.

XXII. Choroiditis at Macular Region.

Fig. 49. Superficial Choroiditis at Macula.

,, 50. Choroiditis at Macula.

,, 51. Do. at Macula. Old.

„ 52. Do. do. do.

XXIII. High Myopia.

Fig. 53. Myopic Crescent (Stationary).

„ 54. Progressive Myopia.

„ 55. Choroiditis and High Myopia.

XXIV. Senile Choroiditis and Post-Xeuritic Atrophy.

Fig. 56. Senile Choroiditis.

„ 57. Post-Xeuritic Atrophy. Cicatricial Changes at Macula. Choroidal Atrophy.

XXV. Retinal (Edema and Membranous Formation in Retina.

Fig. 58. Choroiditis. (Edema of Retina.

„ 59. Do. Membranous Formation in Retina.

XXVI. Choroido-Retinal Sclerosis.

Fig. 60. Choroido-Retinal Sclerosis, or Diffuse Choroido-Retinitis.

XXVII. Choroido-Retinal Sclerosis.

Fig. 61. Choroido-Retinal Sclerosis, or Diffuse Choroido-Retinitis.

XXVIII. Retinal Atrophy with Secondary Pigmentation.

Fig. 62. Atrophy of Retina with Secondary Pigment Changes.

XXIX. Diffuse Choroiditis.

Fig. 63. Diffuse Choroiditis. “ Map-Like ” Choroiditis.

XXX. Rupture of Choroid.

Fig. 64. Rupture of Choroid.

,, 65. Do. do.

XXXI. Papillitis.

Fig. 66. Papillitis (Subsiding).

„ 67. Papillitis.

„ 68. ,, with Haemorrhages on Disc. Retention of Physiological Cup.

„ 69. Papillitis (Disc much Swollen).

LIST OF ILLUSTRATIONS.

XYll

PLATE

XXXII.

XXXIII.

XXXIV.

XXXV.

XXXVI.

XXXVII.

XXXVIII.

XXXIX.

XL.

XLI.

XLII.

Papillitis. Post-Xeupitic and Simple Atrophy.

Fig. 70. Papillitis. With “Ridging” of the Retina.

,, 71. Post-Neuritic Atrophy. Atrophy of Choroid near Disc.

„ 72. Post-Neuritic Atrophy.

„ 73. Primary Atrophy.

Leukemic Retinitis. Papillitis.

Fig. 74. Leukaemic Retinitis.

„ 75. Papillitis. Much Swelling. Vision Unaffected. Subsidence.

Thrombosis of Central Vein.

Fig. 76. Thrombosis of Central Vein.

„ 77. Do. do.

Retinitis with Haemorrhages.

Fig. 78. Retinitis. Hemorrhages and White Dots. Recovery.

„ 79. Retinal Hemorrhages. (Thrombosis 1)

Albuminuric Retinitis and Neuro-Retinitis.

Fig. 80. Retinitis at Macula. Hyaline Thickening of Artery.

,, 81. Neuro-Retinitis.

Albuminuric Retinitis.

Fig. 82. Albuminuric Retinitis.

„ 83. Retinitis. Without Implication of Disc.

,, 84. Albuminuric Retinitis. “ Star Figure” at Macula.

Stellate Figure at Macula and Post-Neuritic Atrophy.

Fig. 85. Stellate Figure at Macula of Unusual Character.

„ 86. The Same Eye. Two Months Later.

„ 87. Post-Neuritic Atrophy.

Subiiyaloid Haemorrhage.

Fig. 88. Sub-Hyaloid Hemorrhage at Macula.

,, 89. The Same Eye. Fourteen Days Later.

Changes in Vessel Walls. New Vessels in Vitreous.

Fig. 90. Degenerative Change in arterial walls.

„ 91. New Vessels in the Vitreous.

Embolism of Central Artery.

Fig. 92. Embolism of Central Artery.

„ 93. Do. do. Modified by the presence of a Cilio-Retinal

Vessel.

Retinitis Pigmentosa. Pigmentation from Choroido-Retinitis.

Fig. 94. Retinitis Pigmentosa.

„ 95. Choroido-Retinitis. With unusual Pigmentation.

XV111

LIST OF ILLUSTRATIONS.

PLATE

XLIII. Eetinitis Pigmentosa.

Fig. 96. Retinitis Pigmentosa.

XLIY. Retinitis Pigmentosa.

Fig. 97. Retinitis Pigmentosa. With little Pigment Deposit.

XLY. Cicatricial Bands on Fundus.

Fig. 98. Choroiditis. Secondary Pigmentation of Retina. Formation of Cicatricial
Bands.

„ 99. Cicatricial Bands on the Fundus.

XLYI. Detachment of the Retina.

Fig. 100. Detachment of the Retina.

Do.

do.

XLVII. COLOBOMA OF DISC. GLAUCOMA SIMPLEX.

Fig. 104. Partial Coloboma of Disc.
„ 105. Glaucomatous Cup.

„ 106. Do.

107. Do

THE FUNDUS OCULI.

INTRODUCTION.

The Ophthalmoscope not only enables us to study the progress of
diseases of the fundus, but it frequently leads to the recognition of
morbid conditions of the general system, or of parts remote from
the eye. Moreover, the fundus oculi, owing to its complex struc-
ture, and the conditions under which it is seen, presents an
unrivalled field for the study of pathological processes in living
tissues.

In the retinal vessels are exposed to view the minute rami-
fications of a terminal artery and vein, in close connection with
the cerebral circulation ; in the optic disc there is presented to
us an optical section of a cranial nerve ; in the retina we see
a highly organised membrane, which, in part at any rate, is a
direct continuation of that nerve ; while in the choroid there is
spread out before us a membrane so vascular that its colour is
almost that of the blood. Nor is this all — these various structures
are seen through the dioptric system of the eye, which, acting like
the low power of a microscope, presents them to us enlarged about
fifteen diameters.

The retinal vessels may present changes of the gravest import
to the integrity of the eye. But besides this they may afford
evidence of irregularities in the general circulation, of widespread
vascular disease, or of alterations in the character of the blood.

The state of the optic disc may prove to us that the path of
conduction between the retina and the nerve centre is interrupted,
but it may also indicate the existence of disease, docalised in the
l

INTRODUCTION.

brain or spinal cord, or disseminated throughout the nervous
system.

Inflammation of the choroid is much more common than any
other affection of the fundus, and frequently leads to loss of sight.
Perhaps it is on this account that its general importance is apt
to be overlooked, but it should not be forgotten that it often affords
valuable corroborative evidence of the presence of syphilis or
of tuberculosis.

The great liability of the choroid to chronic inflammation is
probably due not only to the large amount of blood contained in
its tissue, but also to the fact that the circulation is very sluggish.

Degenerative, no less than inflammatory, changes in the
choroid or retina have more than a local importance, for they may
indicate disease of important organs, degenerative processes in
the vascular system, or widespread deterioration of tissue.

Familiarity with morbid conditions of the fundus is therefore
hardly less essential to the general physician than to the specialist,
a fact that has in recent years been more and more recognised.
It is not, however, so generally remembered that an essential pre-
liminary to the diagnosis of morbid conditions of the fundus is
a thorough knowledge of its normal appearance. This can be
attained only after some experience, since even normal fundi differ
from each other within rather wide limits. For this reason a
relatively large share of the following pages will be devoted to the
consideration of what may be conveniently called “physiological
variations.”

If the variations of the normal fundus are numerous, those
presented by pathological conditions are still more so ; for these
latter are generally the product of several factors, the relative
prominence of which varies in different cases. Hence the physician
will not learn much by examining only such cases as are most
likely to be met with in medical practice, but must embrace
every opportunity of becoming familiar with all the appearances
that the fundus may present.

INTRODUCTION.

The primary object of this work is to advance the study of
ophthalmoscopic diagnosis. Questions of treatment and prognosis,
and the relation of fundus changes to general conditions, will,
from time to time, be touched upon, but the treatment of affec-
tions of the fundus cannot, with advantage, be considered apart
from ocular therapeutics in general, while a physician alone
would be competent to write a complete treatise on medical
ophthalmoscopy.

The method adopted will be to illustrate the text by coloured
representations of the fundus, drawn from living cases. These
drawings necessarily occupy a prominent place in the book, but
it is hoped that the reader will look upon them as illustrating the
text, and not merely use the text to explain the drawings.

The cases have, for the most part, been selected as typical
examples of fairly common conditions. In illustrations of the
fundus it has been too much the custom to devote great care
to depicting the condition under consideration, while other parts
of the fundus have been represented in a sketchy, diagrammatic,
or conventional manner. Every part of every fundus may be
important, and the attempt has therefore been made to depict
the conditions present exactly as they appeared, without ex-
aggerating particular parts or slurring over others.

The drawings of the fundus have been executed from nature
by an artist, and all (except Plate II., Fig. 6, Plate IX., Fig. 26,
and Plate XX., Fig. 46) were made under the direct supervision of
the writer.

The direct method has been employed, except for the drawings
on Plate XXIII. As these represent cases of high myopia, the
indirect was found to be more suitable.

Most of these pictures represent more of the fundus than can
actually be seen at one time by the direct method. Without
altering the position of the mirror it is impossible to see more than
the optic disc, and a narrow zone round it. But different parts can
be viewed in quick succession, and it is usual in drawings to piece

INTRODUCTION.

these together so as to form a single picture. The practice is too
obviously convenient to need defence.

The drawings were made by the aid of artificial light, and
appear to the best advantage when viewed under the same
conditions.

They are life-size, but it must be remembered that the apparent
size of the ophthalmoscopic image may vary in different observers.
The actual retinal image received by the observer must be of the
same size as the part of the patient’s eye which produces it (if both
his eye and that of the patient are emmetropic and of the same
dimensions). But the apparent size of the mental picture will
depend upon the distance to which the observer projects his
retinal image.

Fig. 1. — Diagram to illustrate the enlargement of the image in direct
ophthalmoscopic examination.

This will be evident from Fig. 1, in which A represents the eye of the observer, and B
that of the patient. Both are emmetropic and of identical dimensions, and they have a
common principal axis, x y. Let a b represent a portion of the patient’s eye seen by A.
b lies on the principal axis of B, therefore its image, V , is on the principal axis of A.
Let a ray, a o, from a pass through the optical centre o, then all other rays from a will,
after emerging from the eye, be parallel to a o. Let one of these, a o', pass through o, the
optica] centre of A, then it will be unrefracted, and will cut the retina at a. This point
will give the position of the retinal image of a.

It will be found that the image a b' is equal to the object a b. For since a o and a o
are parallel, the angles at o and o are equal, and since the distance from o and o' to their
respective retinae are equal, a b = a' V.

It is evident that A may project the retinal image a V to bv b2, or b3, or to any other
distance, and that the size of the virtual image will vary accordingly.

Since the apparent size of the ophthalmoscopic image may not
be the same to different observers, it is necessary in describing

INTRODUCTION.

appearances to use a standard of measurement obtained from the
eye under observation. The best unit for this purpose is the
diameter of the optic disc. For example, we may describe a
patch of choroiditis as being 3 dd. from the macula, and having
a diameter of For smaller measurements the diameter of the
main vessels may be used.

To facilitate measurements of this kind the writer, in conjunc-
tion with Mr. Sydney Stephenson, designed a fundus-gauge,
consisting of a rectangular network of fine wires, which, when
attached to an ophthalmoscope, threw its shadow on the fundus,
thus mapping it out into squares. The practical utility of
the instrument is somewhat diminished by the impossibility of
rendering these shadows visible on the disc.

Opposite each chromolithograph will be found a short account
of the case, together with the chief points which are illustrated
by it. If information is required in respect of any particular
ophthalmoscopic appearance, a reference to the index will show
the part of the text in which the condition is discussed, and the
drawings in which it is depicted.

It must not be supposed that any picture, however accurate,
can equal in beauty the actual ophthalmoscopic image. The
brilliancy and freshness of the living fundus cannot be reproduced.
Some appearances vary with the slightest alteration in the
direction of the incident light, and the attempt to fix them in a
drawing gives an unnatural hardness. Others depend on
differences in level, or on one tissue being viewed through
another, which, although presenting no perceptible opacity,
may not be perfectly transparent. A faithful representation
of these is difficult. Of course, such appearances as depend
upon rhythmical changes in form, as for example pulsation,
or upon apparent change of relative position, as in parallactic
movements, cannot be depicted at all. For these reasons the
fundus can only be adequately studied by means of the ophthal-
moscope.

INTRODUCTION.

Much, however, will be learnt from these pictures by anyone
who will use them as a means to an end, and not as the end itself.
To such an one they will explain many things which he will
remember to have seen and not understood ; they will in the future
enable him both to see and to perceive.

This work is, to some extent, an amplification of the “ Lantern ”
Lectures which I have delivered at the Royal Westminster
Ophthalmic and at St. George's Hospitals, and such of my readers
who attended those lectures will recognise many of the lantern
slides. Many new drawings have, however, been added, and the
text is much fuller than was possible in a course of lectures.

PART I

PHYSIOLOGICAL VARIATIONS.

CHAPTER I.

THE NORMAL FUNDUS.

My object is not so much to lay before my readers examples of rare
conditions of the fundus, as to show them how the more common
appearances, both normal and pathological, are produced. Physio-
logical variations will therefore receive an unusual amount of
attention, and abnormal conditions will be considered not so much
from the standpoint of the completed picture, as from that of the
details which go to produce it.

By dealing in this manner with the material at our disposal,
it is hoped that the reader may be led to abandon the
pernicious belief that diagnosis consists merely in giving a name
to an ophthalmoscopic picture. Such a picture is necessarily the
sum of many factors which may be combined in very different
proportions. Unless this be borne in mind, there is a twofold
possibility of error. On the one hand, a single name may be
used to include a number of conditions which, presenting some
features in common, may differ in many important respects.
On the other hand, different names may be given to ophthal-
moscopic appearances which are the result of identical patho-
logical processes.

Diversity of appearance is not confined, however, to patho-
logical conditions : the normal fundus-image is also the sum of
several variable factors ; hence no two fundi are exactly alike, and
it is therefore impossible to take a single type as the normal
standard, and to class all departures from it as abnormal.

Even if we exclude from present consideration such physio-
logical variations as conspicuous abnormalities in the vessels,
opaque nerve fibres, and striking irregularities in the shape of
2

THE NORMAL FUNDUS.

the optic disc, we still have scope for wide variation in the
extent to which the choroidal vessels are visible, in the colour of
the fundus, in the amount of retinal-reflex, and in many other
minor points. Even experienced observers often find it difficult
to discriminate between a physiological variation and a slight
pathological change.

ac.

Fig. 2. — Horizontal section of eyeball. Drawn to scale from measurements
of numerous specimens (reduced from Arlt and Efinger’s “ Horizontal Durch-
schnitt ”).

ac. Anterior chamber ; a. angle of anterior chamber ; pc. posterior aqueous
chamber ; i. iris ; V. vitreous ; l. lens ; c. ciliary body ; art. cent, central vessels of
retina.

The “ fundus ” may be roughly defined as the inner surface of
the posterior hemisphere of the globe. It will simplify the
subject if we consider separately the factors which contribute to
the ophthalmoscope image, — first of the fundus generally, and
then of two special parts of the fundus, namely, the optic disc
and the yellow-spot.

Each tunic of the eyeball contributes something towards the

SCLEROTIC.

ophthalmoscopic image of the fundus, but by far the largest share
is due to the choroid.

The sclerotic may be said to constitute the panel on which our
picture is painted. By virtue of its rigidity it helps to maintain
the globular shape of the eyeball, and affords a firm leverage for
the ocular muscles, which are attached to it. It is thickest
posteriorly, where it is continuous with the dural sheath of the
optic nerve, and becomes gradually thinner anteriorly, until, near
the cornea, it is slightly thickened by reinforcements from the
tendinous insertions of the muscles. The sclerotic is pierced
around the optic nerve by the two long ciliary, and the numerous
posterior ciliary arteries, and near the cornea by the perforating
branches of the anterior ciliary arteries, while, about the equator,
there traverse it obliquely from before backwards, and from within
outwards, veins which correspond in function with the arteries ;
these, from the arrangement of their converging tributaries, have
been called venrn vorticosse (Fig. 5 Vv.).

The sclerotic itself is not usually visible, as it is covered by the
nearly opaque choroid. But in all eyes except the darkest, and
possibly in them also, it has some influence on the ophthalmoscopic
picture, since a certain amount of light reaches it through the
choroid, and, being reflected, serves to lighten the fundus. The
extent to which this occurs is in inverse proportion to the amount
of pigment in the choroid and retina.

In the albino there is no pigment, and the sclerotic is then
visible as a white surface between the choroidal vessels. The
vision of albinos is always defective, and they suffer from nystag-
mus ; for this latter reason it has not been possible to obtain a
painting of the fundus. But a similar appearance is often met
with in the eyes of fair persons, although, as a rule, it is not equally
marked over the whole fundus. A good example of such a fundus
is to be seen in Plate III., Fig. 7.

The sclerotic is, however, best seen where the choroid is absent,
either as the result of a congenital defect, as jn coloboma, or

THE NORMAL FUNDUS.

owing to its destruction by disease. The former of these conditions
is seen in Plate IX., Figs. 26 and 27, and the latter in Plates
XVI., XXI., XXII., and in many others. When thus exposed,
it presents a brilliant white surface, unlike the dull dead-white
colour of inflammatory exudation.

In deeply pigmented eyes, on the contrary, the choroidal
vessels, as a rule, are not visible. Little light is reflected from
the sclerotic, and the fundus consequently has a dull, sombre
appearance (Plate II., Fig. 6). In the eyes of dark races, the

Fig. 3. — Perpendicular section of choroid. (From a specimen prepared by
Mr. Treacher Collins.)

a. Pigment layer of retina ; b. choroid ; c. lamina fusca.

small amount of light reflected from the fundus sometimes renders
satisfactory ophthalmoscopic examination difficult. Plate XLII.,
Fig. 95, shows the eye of a half-caste, and although it represents
a fundus which is abnormal, it will serve to show the colour which
is frequently seen in dark races.

Between the sclerotic and the choroid is some loose cellular
tissue — the suprachoroidea (Fig. 3, c). The outer layers of this,
which are deeply pigmented, adhere firmly to the sclerotic, and are

CHOROID.

sometimes called by a separate name, the “ lamina fusca.” The
spaces in the suprachoroidea are said to be lined by an endothelium,
and probably form part of the lymphatic system. The ciliary
nerves which supply the uveal tract pierce the sclerotic round the
optic nerve entrance, and run in the suprachoroidea.

The choroid takes by far the largest share in the production of
the ophthalmoscopic picture. Owing partly to the amount of
pigment it contains, and partly to the fact that it is composed to a
large extent of blood vessels, which become collapsed after death,
its minute anatomy is less easily demonstrated than that of the
retina. For our knowledge of this subject we are largely indebted
to the researches of Iwanoff and Sattler.

The pigment epithelium usually adheres to the retinal surface
of the choroid, although a study of its development proves that it
really belongs to the retina. It will be described later on. Next
to the retinal pigment lies the lamina vitrea ; this is usually
described as structureless, but Sattler has recently shown that
its deep surface is marked by a network of fine interlacing lines.
Next comes the capillary layer, or “ chorio-capillaris.” These
capillaries are the largest in the body, and the oval nuclei in
their walls are very conspicuous. When more than one layer of
capillaries can be distinguished, the more superficial contains
the finest vessels. This is shown in Fig. 4, which is from the
choroid of a rabbit.

The richness of the capillary network varies in different eyes,
and in different parts of the same eye, being almost always
greatest near the posterior pole, while towards the periphery the
network becomes more open.

Between the chorio-capillaris and the larger vessels which feed
it, we have what might be called an intervascular layer, consisting
largely of elastic fibres, and containing as a rule no pigment. The
more external layer is made up chiefly of arteries and veins lying
in a deeply pigmented stroma. The position of the vessels in these
layers is shown in Fig. 3, but they are abnormally conspicuous

THE NORMAL FUNDUS.

owing to the choroid being congested. The specimen from which
the drawing was made, was taken from a case of recent injury.

Perivascular lymph sheaths accompany the veins and become
continuous with the intercapillary spaces.

Throughout the choroid are found unpigmented cells which
appear to vary greatly in number. In the outer layers are also
pigmented cells which vary much in form, size, and in the
amount of pigment which they contain.

Fig. 4. — Choroidal capillaries seen in horizontal plane. (From an injected
specimen by Mr. Jno. Griffith.)

The uveal tract becomes modified anteriorly to form the ciliary
processes and muscle, and, still more anteriorly, the iris, but with
the anatomy of these parts we are not now concerned.

The greater part of the uveal tract derives its blood supply

CHOROID.

from the posterior or short ciliary arteries (Fig. 5, Ah), which pierce
the sclerotic round the optic nerve. The ciliary region is supplied
by two long and numerous anterior ciliary arteries. The former
(Fig. 5, Al ) pierce the sclerotic one on either side of the optic nerve,
then course forward between the sclerotic and choroid. The
perforating branches of the anterior ciliary arteries, on the other
hand, pierce the sclerotic about 5 mm. from the corneal margin.

No distinction can be made between the smaller arteries and

Fig. 5. — Diagram of the vessels of the choroid. (Graefe n. Saemisch.)

A a. Anterior ; Al. long — A b. short — ciliary arteries ; Vv. venae vorticosae ;

Cirri, circulus iridis major ; i. iris ; Pc. ciliary process ; Oc. ciliary muscle.

veins of the choroid, but as the latter unite into larger trunks they
assume a peculiar appearance owing to their being arranged in
regular bold curves. The separate veins are nearly parallel but
gradually converge, an arrangement which has led to their being
called venae vorticosae (Fig. 5, Vv) ; finally all the veins are collected
into six or eight large trunks which pierce the sclerotic somewhat
obliquely near the equator.

THE NORMAL FUNDUS.

The ophthalmoscopic appearance presented by the choroid is
largely dependent on the pigment-layer of the retina. It will
therefore be necessary in this place to consider this layer. Ifc
consists of a single layer of hexagonal cells, arranged in juxta-
position as in a tessellated pavement. Each cell contains pigment
granules which are more numerous at its periphery than in its
centre. From each cell a fine filament passes for a short distance
between the rods and cones, constituting the adjacent layer of
retina (Max Schultze).

When there is a moderate amount of pigment in this layer, it
hides all details of the choroid from view, but
the great vascularity of the capillary layer gives
to the fundus an almost uniform red colour, the
brightness of which depends on the amount of
light which can penetrate the choroid, and be
reflected from the sclerotic. In Plate I., Fig. 1,
Fig. 6.— Pigment epi- we gee a rather bright fundus colour : in Plate

thelium of retina.

(Graefe u. Saemisch.) vl., Fig- 17? and Plate X., Fig. 29, it is much
duller, while in eyes which are deeply pigmented,
the fundus is almost slate coloured (see Plate II., Fig. 5, and
Plate XLII., Fig. 95).

The retinal pigment itself may be visible, producing in dark
eyes the appearance of very fine stippling. Occasionally an analo-
gous condition is met with in fair eyes, when the fundus has the
appearance of being peppered over with fine grains of gun-
powder.

When the retinal pigment is less abundant the observer is able
to see a certain distance into the choroidal substance. The
appearance will then depend upon the amount of pigment in the
stroma of the choroid ; this is usually proportionate to the
pigmentation of the pigment layer of the retina, but exceptions
are not uncommon.

When there is no pigment in the choroidal stroma, as in
albinos, the choroidal vessels are visible on the white background

RETINAL PIGMENT.

of the sclerotic, which receives a mere tinge of red, probably from
the capillary layer of the choroid. The constant association of
nystagmus with this condition has, unfortunately, hitherto pre-
vented me from obtaining an accurate drawing. Choroids which
are but slightly pigmented are, however, comparatively common,
and in such cases a variable number of choroidal vessels are seen
separated by interspaces which are lighter than the vessels, and
sometimes almost white (Plate III., Fig. 7).

No difficulty should ever arise in distinguishing choroidal from
retinal vessels. The former are more numerous, of larger size,
and so close together that the interspaces are often narrower
than the vessels. They run in nearly parallel lines, and frequently
anastomose ; they do not, like the retinal vessels, diminish in size
towards the periphery. No distinction can be made between the
arteries and the veins of the choroid. The absence from the
choroidal vessels of the central light-streak, seen in most of the
retinal vessels, gives them a flat riband-like appearance, which is
in striking contrast to the cylindrical form of the retinal vessels.

The choroidal vessels are usually more easily recognised at the
periphery than at the centre of the fundus, but even when they
are visible over the whole of the rest of the fundus, none are to be
seen within the area of the macula.

Loring1 attributes the chief share in the production of these
differences to the superficial capillary layer of the choroid. But
the facts seem to be more in accord with the generally accepted
view, which is that they depend upon variations in the pigment
layer. The choroidal vessels are, as a rule, much more visible in
fair than in dark eyes, and the pigmentation of the fundus
shows some correspondence with that of the skin. It is quite
true, as already pointed out, that individual exceptions to this
rule are not infrequent, but that such are merely personal
peculiarities is at once evident if we compare the eyes of dark
and fair races.

1 “ Text-book of Ophthalmology.

THE NORMAL FUND UN

There does not seem to be any evidence that the closeness of
the capillary network varies to any appreciable extent in different
individuals. It is true that the network is more open towards the
periphery than near the centre, and some colour is thus lent
to Loring’s view, but it is impossible to conceive of it varying in
adjacent areas to a degree which would be necessary to account
for the differences in the ophthalmoscopic appearances.

Moreover, the evidence afforded by disease leading to destruc-
tion of this capillary layer seems to show that its effect is not to
conceal the larger vessels, but to give the fundus a red tinge as if
it were covered by a transparent red veil.

There is usually a relation between the pigmentation of the
retinal pigment layer and that of the choroidal stroma. Some-
times, however, eyes with deeply pigmented choroids have the
retinal pigment sufficiently thin to allow the choroidal vessels to
be visible. We then have the appearance known as the “ ch oroide
tigree,” in which the choroidal vessels are seen as pale bands
separated by spaces of dark colour (Plate III., Fig. 8). In dark
fundi this can usually be seen at the periphery, and not unfre-
quently in other parts.

Local excrescences of pigment in the form of isolated dots are
not uncommon, and they can in no sense be considered pathological.
As we shall see later on, some pigment is generally present round
the circumference of the disc.

A less common form of pigmentation is shown in Plate X.,
Figs. 28 and 29. In this a portion of the fundus, usually sector-
like in shape, has scattered over it groups of pigment dots, which
may be black or dark-brown. For the most part the individual
dots are angular or irregular in shape, rather than round, and their
diameter is usually less than that of the main retinal vessels. The
dots are collected into groups, the fundus between the groups
presenting nothing abnormal. Most of them appear to lie deeper
than the retinal vessels, although there are occasional exceptions
to this. They differ from pathological pigment deposits by the

RETINA.

absence of any decoloration of the portion of the fundus on which
they rest, and by the sharp limitation of the individual dots, each
having a well-defined outline, and being quite separate from its
neighbours. Vision is unaffected, and there seems to be no
tendency for the condition to alter in any way.

The cases depicted in Plate X., Figs. 28 and 29, were under the
observation of Mr. Stephenson, who kindly permitted me to have
drawings made. They have been published by him with another
case,1 and I understand that he has since seen four others.

A similar case has been published by Jaeger in his Atlas. He
considered it to be an early stage of retinitis pigmentosa.

Larger areas of pigmentation are occasionally met with in eyes
which are presumably healthy. They are brown, rather black,
and tend to have a regular oval or circular outline. They are
probably analogous to moles on the skin. Dodd“ has published
a case of this kind, with an illustration of the ophthalmoscopic
appearance.

The retina , which now claims our attention, is the innermost
coat of the eye-ball, and may be considered as the end organ of
the optic nerve. It is, therefore, functionally of great importance.
It takes, however, a smaller share in the formation of the ophthal-
moscopic picture than either of the other tunics, owing to its
transparency.

The retina is attached to the optic disc, its superficial layer
being directly continuous with the fibres of the optic nerve.
Anteriorly it terminates in the ciliary region in a jagged margin,
the ora serrata, which adheres firmly to the uveal coat. Between
these points it is kept in contact with the choroid merely by the
pressure of the vitreous, except at the yellow spot, where it adheres
slightly to the choroid.

Under the microscope the retina can easily be seen to consist
of several layers, which differ considerably from each other. The
examination of the minute structure of these, and of their connec-

1 Trans. Ophtli. Soc., vol. xi., p. 77.

2 Trans. Ophth. Soc.,y ol. xv., Plate IX.

THE NORMAL FUNDUS.

tions with each other presents, however, great difficulties, and
although much has been discovered in recent years with regard
to them, there are still many points that remain obscure.

The different layers from without inwards are enumerated in
the following table.

The numbers correspond with those in Fig. 7.

Pn
H
P
P
: P

2.
f 3.
4.

Ph j
O

JO.

Pigment Layer.

Bacillary Layer (rods and cones).

External Limiting Membrane.

External Nuclear Layer.

(a.) Nuclei of rods and cones.

(b.) Fibres of do. (syn. external fibrillar layer).
External Molecular Layer {syn. internuclear
layer).

Internal Nuclear Layer.

Internal Molecular Layer.

Layer of Nerve Cells.

Layer of Nerve Fibres.

Internal Limiting Membrane.

1. The pigment layer has already been dealt with. It sends down
processes between the elements of the next layer to an extent
which is believed to increase with the amount of light entering
the eye. Notwithstanding this close connection with the bacil-
lary layer, in microscopical preparations it often becomes separated,
and when the retina during life becomes detached from the choroid
the pigment layer usually remains in contact with the latter.

2. The bacillary layer is so called because it consists of fine
parallel bodies, which were named bacilli before bacteriological
investigations had given a different significance to the word. It
is now more frequently called the layer of rods and cones.

The elements composing it are of two kinds, the more numerous
are straight bodies, of uniform thickness; these are the “ rods/' The
other elements — the cones — are seen interspersed amongst the

RETINA.

rods at almost regular intervals. They are shaped like champagne
bottles (Fig. 8), and have their narrow ends directed towards the
pigment layer.

The cones obviously consist of two portions, which correspond
respectively with the body and neck of the bottle. The rods also
show a division at the same level into an inner and outer segment.

In the peripheral parts of the retina the cones are separated
from each other by about three times their diameter, but, as the

3
•4

Fig. 7. — Perpendicular section through human retina. The numbers refer
to the various layers as described in the text. (From a preparation by Mr.

Jno. Griffith.)

region of the macula is approached, they become more numerous,
each cone being now surrounded by a ring of rods which separates
it from its neighbours. It is usually said that within the macula
itself cones alone are present. This, however, is denied by
Borysiekiewicz.1 He describes the rods as gradually assuming
the characteristics of the cones as the fovea centralis is approached,

1 “ Weitere Untersuchungen liber den feineren Bau der Netzhaut,” 1894.

THE NORMAL FUNDUS.

Rods & Cones <

Ext. limiting memb.

External
Nuclear layer

Ext. Molecular l.

lnt. Nuclear

hit. Molecular <

and he considers that the elements at the fovea should be looked
upon as rods and not as cones.

3. The external limiting membrane is so named in contradis-
tinction to the internal limiting membrane which lies on the
vitreous surface of the retina. It is visible under the microscope
as a sharply defined line. Its structure possesses no features of
importance.

4. The external nuclear layer (sometimes called external granu-
lar) has the appearance of being divisible into two parts, an outer

which consists chiefly of nuclei, and an
inner which is made up almost entirely of
parallel fibres continued from the rods and
cones. It must, however, be remembered that
these fibres traverse the whole of this layer,
and indeed pass through all the layers to
reach the nerve cells, although, in the inner
layers they are less easily demonstrated.

This part of the retina in microscopical
sections contains numerous vacuoles, which
are more conspicuous than the fibres. The
latter, like all the fibres in the retina, can
only be well seen after special treatment.

The nuclei of this layer are round or
oval bodies, developed on the fibres from
the rods and cones. The two sets of fibres
differ from each other in the thickness and
in the position and size of their nuclei.

5. & 7. The outer and inner molecular layers. — These two layers
have been described in various ways, and there seems still to be
much doubt as to their structure. They contain numerous small
oval and round cells and an anastomosing network of fibres, held,
on the one hand, to be nervous, and, on the other, to consist of
connective tissue only. The inner layer is much thicker than the
outer, but otherwise they resemble each other.

Nerve cells •

Nerve fibres

Extremities of fibres of Muller
forming Internal limiting
membrane

Fig. 8. — Diagrammatic sec-
tion of retina. (Modified from
Merkel, Arch. f. Oplith., Leip-
zig, bd. xxii., p. 2.)

RETINA.

6. The inner nuclear layer resembles the nuclear portion of the
external nuclear layer (4). A connection has been demonstrated
between the nuclei of this inner nuclear layer and the nerve cells
in the next layer (8) ; concerning its connection with the more
external layers there is much uncertainty.

8. The layer of ganglionic nerve cells consists of large multipolar
cells from each of which one process passes into the layer of nerve
fibres. From the other surface project a number of processes,
varying from one to four, most of which appear to be lost in the
adjacent inner nuclear layer ; a few, however, can be traced as far
as the external nuclear layer.

9. The layer of nerve fibres is thickest near the disc, and stops
short before reaching the ora serrata. It consists of fibres which
are continuous with those of the optic nerve, but which differ
from them in having lost their outer coating of the white matter
of Schwann, or medullary sheath. They are, in consequence, thin
and transparent. The larger vessels of the retina lie in this layer.

10. The internal limiting membrane is a thin not conspicuous
membrane, which is usually described as being formed by the
expanded extremities of the fibres of Muller.

The fibres of Muller, to which reference has just been made, are
not shown in the figure, they are straight filaments, which pass
vertically through the intervening layers from the external to
the internal limiting membrane. They have usually been con-
sidered as forming part of the connective tissue framework of the
retina. Borysiekiewicz1 has, however, shown that they are directly
continuous with the bases of the cones. And if this is really
the case, it is probable they constitute nerve organs of great
importance.

The structure of the retina is somewhat modified at the macula.
This will be considered later on.

The vessels of the retina are branches of the central artery
and vein. Those that are of sufficient size to be visible with the

1 Lnc. cit.

THE NORMAL FUNDUS.

ophthalmoscope lie in the fibre layer, and fine offshoots pass from
them into the deeper layers. The veins, like those of the choroid,
are surrounded by perivascular lymph channels.

The great vascularity of the choroid, its close proximity to the
layer of rods and cones, and the fact that even superficial choroidal
disease soon impairs vision, would seem to indicate that the
choroid plays a very important part in the nutrition of the retina,
probably through the medium of its pigment layer. That the
supply of arterial blood through the central vessel is of more
vital importance is proved by the fact that when the latter
becomes plugged by a clot, there is instantaneous and total blind-
ness, which is permanent, unless the circulation be quickly
restored.

One result of the relative position of the vessels and the
sentient layer is that the visual field lias gaps in it corresponding
to the larger vessels. These are not observed under ordinary
conditions, because we are accustomed to their presence, and there
are no large vessels near the yellow spot where vision is most
acute. If, however, light is thrown into the eye obliquely through
the sclerotic, so that the shadows of the vessels fall upon nerve-
elements which are unaccustomed to them, they are seen and are
projected as dark branching lines, like the branches of a leafless
tree (“ Purkinje’s Figures ”).

Although the main retinal vessels usually avoid the yellow spot
region, there is here a very fine network of smaller vessels, which
can also be viewed subjectively in a manner which will be described
later.

Another result of the position of the sentient layer is that
vision is impaired by the slightest loss of transparency in the
superficial layers.

We pass now to the effect produced on the ophthalmoscopic
picture by the retina. Owing to its almost perfect transparency
(excluding, of course, its pigment layer), the retina itself is usually
invisible in the normal condition, its existence being only rendered

RETINA.

evident by the presence of the blood vessels. These, as already
stated, lie in the fibre layer, sometimes even projecting a little
above the general surface.

Although the retina is not usually visible, its presence is some-
times indicated near the disc, where the fibre layer is thicker
than elsewhere, and also at any point where some of the fibres cross
a vessel owing to the light being caught and reflected, so that we
become conscious of the existence of a fine, grey, gauzy veil, or of
wavy streaks, overlying the red surface. The effect produced is very
variable, and difficult to describe or depict, for the appearance
presented varies with the direction of the incident light, and
therefore with every change in the position of the ophthalmoscope
mirror. Hence any attempt to depict it in a drawing gives an
unnaturally hard result.

The more pigmented the fundus, the more conspicuous is this
retinal reflex, and in very dark eyes, as in Plate II., Figs. 5 and
6, it may extend over the whole fundus, and almost conceal the
red choroidal reflex, replacing it by a grey surface.

Usually, however, this reflex is observed only when the
light strikes the retina at a certain angle, so that it is seen to
shift from one part to another as the mirror is moved ; this
phenomenon is spoken of as the “ shot-silk ” appearance, although
“ watered silk ” would be a more descriptive term.

All these reflex appearances are most marked in young eyes,
and tend to disappear with advancing age ; they are also more
conspicuous under a feeble illumination, and with a concave than
with a plane mirror.

An extreme case of retinal reflex was brought to my notice by
Mr. Stephenson in November, 1891, and has since been published by
him.1 The patient was a boy, aged 9, of rather dark complexion.
The fundus presented a series of bright silvery circles concentric
with the disc margin, their outline being a little irregular and
broken in places. Near the disc they were well defined, but they

1 Trans. Ophth. Soc., vol. xii., p. 115.

THE NORMAL FUNDUS.

became less so, and formed less complete rings towards the peri-
phery of the fundus ; the general arrangement was suggestive of
the waves radiating from a stone thrown into smooth water. Each
band was about twice the thickness of the largest retinal vessels,
and the individual bands were separated by spaces slightly wider,
in which the normal choroidal reflex was visible. They appeared
to lie in front of the retinal vessels. There were also present very
fine straight lines, radiating from the disc, as in Plate III., Fig. 8,
apparently produced by the retinal nerve fibres.

The condition appears to be an extreme example of that
which has been described under the term “ concentric retinal
striation." 1

All these reflex appearances are probably due to irregularities
in the surface of the retina, and possibly are in some way connected
with the folded condition of that tissue during foetal life, a connec-
tion that might also explain the more frequent existence of these
appearances in hypermetropia, which may be looked upon as an
arrest of the normal process of development. For a very full
account of the manner in which such irregularities reflect the
incident light, the reader is referred to Dimmer's work.2

A wisp of the patient's hair coming between the light and
the mirror throws shadows on the retina, which might, by a
careless observer, be mistaken for a retinal reflex ; such hair
shadows, however, ought never to cause any confusion.

Occasionally in eyes which appear to be normal we meet
with minute pale dots, which may be white or yellowish. These
may be single, but are more commonly arranged in clusters as in
Plate IV., Figs. 9 and 10, Plate XI., Fig. 30. Since they have
the appearance of being quite superficial, and are often only to
be seen when the light falls on them obliquely, they probably
do not lie in the pigment layer, but are produced by some
irregularity of surface which reflects the light powerfully.

1 Bristowe, Ophtb. Rev., London, vol. x., p. 322.

2 “Die ophthalmoskopischen Liehtreflexe der Netzhaut,” 1891.

RETINA.

I believe that Marcus Gunn 1 was the first to call attention
to these dots, which he found in all the members of one family,
six in number, whom he examined. His paper also contains a
reference to four other individual cases. The appearance, indeed,
is far from rare, but is easily overlooked, owing to the fact that
the dots readily disappear when the light is thrown full on to
them. From the name of Mr. Gunn’s first case they are some-
times referred to as “Crick’s” dots. Plate XI., Fig. 30, shows the
grouping of some of these spots, but gives an exaggerated idea of
their distinctness ; similar dots, but fewer in number, are to be
seen in Plate IV., Figs. 9 and 10, and Plate III., Fig. 8.

Isolated spots of exceeding minuteness, having an absolutely
metallic lustre, and looking like minute particles of mercury, are
occasionally met with ; it would be impossible to depict these
adequately.

All these punctate conditions will be considered in greater
detail later on.

In the following chapters we shall consider two parts of the
fundus which are of especial importance : the entrance of the
optic nerve — the so-called optic disc ; and the central region — the
macula lutea, or yellow spot.

1 Trans. Ophth. Soc., vol. iii., p. 110.

CHAPTER II.

THE OPTIC DISC.

In order to understand the appearances presented by the disc it is
necessary to have an accurate conception of the anatomy of the
optic nerve.

We need not consider the cerebral connections of the nerve
fibres, but may start from the optic foramen where the nerve
enters the orbit. In the orbit the nerve is slightly slack, thus
allowing of the movements of the globe. About fifteen millimetres
behind the globe it is pierced on its outer side by the central
artery and vein, which travel up its axis to the interior of the
globe, where we will leave them for the present.

The optic nerve will be seen in a longitudinal section
(Fig. 9) to pass through a funnel-shaped opening in the
sclerotic, the larger end of which is directed backwards. To
accommodate itself to this opening, the nerve becomes
considerably reduced in size ; not only so, but at the level of
the posterior surface of the sclerotic it changes its character,
for while behind this point it is white and opaque like
other nerves, it here becomes greyish, and gelatinous in
appearance. This is due to the fact that at this point the white
matter of Schwann, which so far has encased the axis cylinder of
each nerve fibre, ceases, only the more transparent axis cylinder
going on. If the opening in the sclerotic be examined with the
microscope (Fig. 9), it will be seen to be crossed by fibres
derived from the sclera. In fact it is not a single large
opening but a collection of openings like those of a sieve, through
which the bundles of nerve fibres separately pass. The structure
has therefore been named the lamina cribrosa. It has a very

NERVE SHEATHS.

important influence on the ophthalmoscopic appearance of the
disc.

We are in the habit of looking upon the optic nerve as consisting
entirely of nerve fibres passing from the retina to the brain, but
recent investigations 1 have shown that it contains about an equal
number of coarser fibres, in which conduction takes place in the
opposite direction. Although the number of fine centripetal fibres
is very great, the retinal cones are about eight times as numerous.

The nerve is invested in its whole course by a loose sheath.

Fig. 9. — Section through optic nerve and papilla.

This is derived from the intracranial dura mater, which at the optic
foramen is also continuous with the periosteum of the orbit.
Anteriorly this dural sheath blends with the sclerotic. Closely
investing the nerve is the less conspicuous pial sheath which is
continuous with the pia mater. This sends down processes between
the bundles of nerve fibres, which give off secondary trabeculae, so
that the whole nerve is permeated by a connective tissue frame-

1 Max Knies, “ Relation of Diseases of the Eye to General Diseases,” 1895.

THE OPTIC DISC.

work which is continuous with the pia mater ; a rather thick process
also accompanies the central vessels, forming their connective
tissue sheath. The pial sheath ceases at the lamina cribrosa. The
space between the dural and pial sheaths, called the intervaginal,
or inter-sheath space, is easily visible to the naked eye in the
section of the optic nerve seen after enucleation. Posteriorly this
space is continuous with the sub-arachnoid space within the
cranium • anteriorly it passes up to the sclerotic, extending some-
times into the posterior larger end of the scleral opening, or even
into the substance of the sclerotic itself. It appears to terminate
in a cul-de-sac, but injection experiments have shown that there
are fine channels passing from it into the substance of the nerve
anterior to the lamina cribrosa.

A small process of arachnoid is usually described as passing
a short distance along the nerve adhering intimately to the dural
sheath, but the existence of this is denied by some authorities.1

It is believed that the intervaginal space constitutes a lymph-
channel, the direction of the stream being towards the globe, and
that a return current exists along the connective tissue sheaths
of the central vessels.

The optic nerve is supplied with blood by branches from
the central vessels. Around the entrance of the nerve into the
sclerotic that membrane is perforated by the posterior ciliary
arteries, these give off branches in the substance of the sclerotic,
which, by anastomosing, form a more or less complete arterial
circle — the circle of Haller. From this numerous fine twigs pass
into the nerve in front of the lamina cribrosa, anastomosing with
those which come from the central vessels. In this way there is
formed within the head of the nerve a fine vascular network
connected both with the choroidal and retinal systems, which is not
without influence on the ophthalmoscopic appearance of the disc.
Anterior to this plexus the retinal vessels have no communications
with any other blood vessels.

1 See Gowers, “Medical Ophthalmoscopy,” 3rd edition, 1890.

BLOOD VESSELS.

The ophthalmic artery, of which the central artery of the
retina is a branch, comes off from the internal carotid by the side
of the anterior clinoid process, and enters the orbit through the
optic foramen on the outer side of the nerve. The ophthalmic
vein, into which the central vein of the retina usually opens, runs
into the cavernous sinus, reaching it through the sphenoidal
fissure. It has a very free anastomosis with the facial vein at
the upper and inner angle of the orbit.

Immediately in front of the lamina the nerve passes through

Fig. 10. — Diagram of blood vessels of optic nerve and disc. (Graefe u. Saemisch.)

R. Retina ; Ch. choroid sclerotics ; c. edge of choroidal foramen ; Aci. branch
of posterior ciliary artery.

an opening in the choroid, which usually embraces it closely.
This, unlike the lamina cribrosa, may be considered as a true
opening, although occasionally a few pigmented fibres can be
traced from the choroid into the nerve substance.

Immediately after passing through the choroid, the fibres of
the nerve bend nearly at right angles over the choroidal margin,
and spread out in all directions to form the fibre layer of the
retina. It is to be noted, however, that they are massed most
abundantly above and below, while the fibres on .the outer side,

THE OPTIC DISC.

which go chiefly to the yellow-spot, form a much thinner layer
than those on the inner side of the disc.

The nerve fibres being merely conductors, are of necessity
more numerous near the disc than at the periphery of the fundus,
and their accumulation here causes the head of the nerve to
project above the level of the rest of the fundus, a circumstance
that has led to its being spoken of as the optic papilla.

While the term optic papilla is fairly descriptive of the
anatomical formation of the head of the nerve, that of optic disc,
which is more frequently used, indicates the appearance which it
presents with the ophthalmoscope, at any rate to a casual observer.
To such it appears as a flat surface of circular outline, lying on the
same level as the adjacent fundus. We shall presently see that
a little attention will generally show that the surface is in reality
convex and raised. The optical illusion is, however, generally
very complete, and is probably due to the fact that we look down
an unknown depth into the semi-transparent nerve, and, having
nothing by which we can gauge the level of the apparent surface,
we refer it to the known level of the fundus.

The absence of a definite opaque surface can be illustrated
experimentally. Thus, it is quite easy to throw shadows of
linear bodies on other parts of the fundus in such a manner that
they are clearly visible with the ophthalmoscope. It will be
found, however, that the disc is incapable of receiving such
shadows.

Under no circumstances is it possible to see beyond the
lamina cribrosa. When that structure is visible, the rather
brilliant whiteness of its tissue is mottled by grey spots,
corresponding to the openings of the nerve fibres. This can be
seen in Plate I., Fig. 1, and Plate XLVII., Figs. 106 and 107,
and in many of the other figures. In the normal condition,
however, the greater part of the lamina is hidden from view by
the nerve tissue over it. This forms a translucent substance,
permeated by a rather rich capillary plexus, which gives it a

PORUS OPTICUS.

reddish colour, and impairs its transparency, so that no details
of the structure of the lamina are visible, although the latter
reflects a certain amount of white light.

It will be convenient to consider the disc as consisting of
three separate parts or zones, although all three are not always
to be recognised in a single eye.

First. The central zone, which is usually of white colour,
and contains the central artery and vein, surrounded by a ring
of connective tissue, and frequently by a portion of exposed lamina
cribrosa, which forms the floor of a depression.

Secondly. The intermediate zone, which extends from the
boundary of the central zone to the outermost zone or margin.
This is of an uniform pinkish colour, of a tint which varies much
in different eyes.

Thirdly. The outermost zone or margin, extending from the
edge of the intermediate zone to the commencement of the
general fundus-colour. This may vary from a mere line to a band
of considerable width, encroaching on the fundus on the one hand,
and on the disc on the other.

The central zone in some eyes may be said to be non-existent,
the intermediate zone closely embracing the central vessels (see
Plate II., Fig. 4, Plate III., Fig. 7, Plate V., Fig. 12, Plate VII.,
Figs. 18 and 19, Plate XIII., Figs. 36 and 37, and others). As a
rule, however, the vessels are surrounded by a ring of connective
tissue, which, being comparatively non-vascular, is of paler colour
than the rest of the disc, Plate III., Fig. 8, and Plate X., Figs.
28 and 29.

The transition from the almost white colour of the connective
tissue sheath to the rosy hue of the intermediate zone may be
gradual or abrupt. Sometimes this connective tissue sheath
instead of closely embracing the vessels, presents a funnel-like
opening, so that the vessels can be traced a short distance into the
nerve. The depression thus formed is called the porus opticus,
and is different in appearance from the forms of physiological cup
5

THE OPTIC DISC.

to be presently described (Plate I., Fig. 3, Plate III., Fig. 8,
Plate V, Fig. 13).

It is, however, more common for the lamina cribrosa to be
exposed to view over a portion of the disc adjacent to the vessels ;
in such cases it evidently lies on a deeper level than the inter-
mediate zone, in fact it forms the floor of a depression. This
depression, which is called the physiological cup, or excavation,
presents great variety of size and form, but it can always be
distinguished from a fully-formed pathological excavation by the
fact that, while it only involves a part of the disc, pathological
cupping affects the whole.

Before considering the different varieties of physiological
cupping, it will be necessary for us to digress in order to
see how differences in level can be recognised with the
ophthalmoscope. One of the most striking effects of such
differences is the parallactic movement that takes place when in
the direct method of examination the observer moves his head in
a plane perpendicular to the line of sight. Under these circum-
stances parts that are relatively depressed appear to move in the
same direction as the observer’s head. The phenomenon is
identical with the optical illusion familiar to everyone who has
watched the landscape from the window of a train in rapid motion ;
distant objects then appear to move in the same direction as,
and near ones in the opposite direction to, the train. With the
ophthalmoscope a very slight difference in level gives rise to a
considerable parallax, because the effect is magnified by the
dioptric system of the eye.

When the examination is made by the indirect method, on the
observer moving his head the whole image appears to move in the
opposite direction, and when he moves the lens it appears to move
in the same direction as the lens, but in both cases the more
superficial parts appear to move more than the deeper. It is often
stated that the parallax is more conspicuous with the indirect than
with the direct method, but my own opinion is the reverse of this.

PHYSIOLOGICAL CUPPING.

A rough estimate of the difference in level can be formed
from the extent of the parallactic movement, but for its
accurate measurement lenses must be placed behind the sight-
hole of the mirror in the direct method. A very minute difference
in level of two points will prevent both being seen in focus with
the same lens. A difference of every dioptre of refraction
indicates a difference of 0 3 mm. of level, so that to find the
difference in level of two points, it is only necessary to ascertain the
lens which brings each respectively into focus, and to multiply the
difference between these by 0 3. For example, the edge of a cup
is seen without any lens while it requires a — 3 D to bring the floor
into view, the depth of the cup is 0 9 mm. Again — the refraction of
the edge is 10 D of hypermetropia ( + 1 '0), while that of the floor is
1 '0 of myopia ( — 1 *0), that is a difference of 2 D , the depth of the
cup is 0'6 mm., and so on. The same rule holds good for the
measurement of projections above the plane of the fundus.

Physiological cups differ much in respect of their area, extent,
depth, and position. Perhaps the most common form is that
shown in Plate I., Fig. 2, in which the cup occupies the centre of
the disc, and its outline is nearly circular. In this instance the
edge is rather steep, so that the vessels on reaching it dip down
abruptly out of sight, and reappear, but of course out of
focus, on the floor of the cup. It is not uncommon for the
cup to present a steep edge on the nasal side, while on the
temporal, the floor slopes up gradually to the level of the fundus
(Plate I., Fig. 3, Plate VI., Figs. 16 and 17, Plate XI., Fig. 30,
Plate XXX., Fig. 65). In these instances the cup was of such a
depth that the edge and the floor could not be seen distinctly
simultaneously. Plate I., Fig. 1, is an example of a large but more
shallow cup, and the mottling produced by the lamina cribrosa is
plainly visible. The cup approaches the margin of the disc most
nearly on the temporal side, and, judging by the course of the
vessels, it seems to be less steep here.

The lamina cribrosa when thus exposed to view presents a

THE OPTIC DISC.

white surface mottled with circular grey spots which correspond to
openings in its structure.

Other varieties of physiological cupping are seen in several
figures, but it should be carefully noted that all possess one
feature in common, namely, that they do not involve the whole
disc. The uncupped portion may be only a narrow zone, or a
crescentic area on one side of the disc, but it is always present.
In this respect physiological cups differ essentially from those of
pathological origin, since the latter, when fully developed, always
involve the whole area of the disc (Plate XLVIL, Figs. 105, 106,
107).

The central vessels vary in their relation to the physiological
cup. Most commonly they appear on its floor, run up the
sides, and curve over the margin (Plate I., Figs. 1, 2, 3, and
others). But they may emerge from the uncupped portion of the
disc, or may pierce the edge of the cup. Finally, they may spring
from the centre of the cup floor, and come forward to the level of

the fundus as if no cupping were present. Occasionally they look
as if they were pushed aside by the cup, lying under, and
curving over its steepest edge. In such cases (Plate XI., Fig. 30,
and Plate XXX., Fig. 65), the vessels may at one moment be
almost concealed from view by the overhanging edge, but come
into view on the observer moving his head, owing to the parallactic
movement they then appear to undergo.

Some authorities 1 consider that the physiological cup is not a
true excavation, but that the apparent absence of tissue in front
of the lamina is due to its transparency. If this be the case it

is difficult to see why the vessels should so often dip down
into the apparent excavation, or why the latter should usually
present a sharply defined edge. Moreover, the appearance
presented by the lamina cribrosa in a physiological and in a
glaucomatous cup is almost identical, although the latter is known
to be a true excavation.

1 Loring, “Text-book of Ophthalmology.

COLOUR OF DISC.

Microscopical sections, for example that in Fig. 9, show that in
the area of the physiological cup the tissue of the nerve is thinned,
and that the surface of the disc presents a true depression.

We now pass on to consider the intermediate zone of the
disc. This extends from the central zone to the margin, and
therefore occupies by far the largest part of the disc. It contains
the whole mass of the nerve fibres, together with a plexus of fine
blood vessels, derived from the branches of the central vessels, and
from the circle of Haller (see p. 30). It is by the colour of this
portion of the disc that we judge of the state of nutrition of
the optic nerve. Atrophic changes, when they reach a certain
stage, cause diminution in the capillary circulation, and increased
transparency of the nerve fibres, so that the lamina cribrosa then
becomes more visible, and this part of the disc paler (Plate
XXXII, Figs. 71, 72, 73).

Increased vascularity, on the other hand, occurs in the early
stages of optic neuritis and causes increased redness of the disc,
and diminution in the transparency of its substance (Plate
XXXI, Fig. 66, Plate XXXII, Fig. 70, Plate XXXVI, Fig. 81,
Plate XXXVII, Fig. 84).

In order to recognise pathological changes in the colour of the
intermediate zone it is of course necessary to be familiar with
the variations which it may present in health, and these are very
numerous.

As already explained, the colour of this portion of the disc is
mainly due to its capillary circulation. The transparency of the
nerve fibres not only allows the red tint or capillary blush to be
visible, but it also permits a certain amount of light to be reflected
from the surface of the lamina. The closeness of the capillary
network circulation varies in different individuals. It is probable
that the transparency of the nerve fibres also does so, and there
are possibly other structural differences which affect the colour.
Apart from these, the apparent tint of this portion of disc is
influenced to some extent by contrast with the colour of the

THE OPTIC DISC.

adjacent fundus. Other things being equal, a disc will appear
lighter when the fundus is very dark.

If, for the present, we exclude from consideration discs which
may be considered exceptional, we shall still see that there is great
variation. The most usual colour is a rosy tint only slightly paler
than the rest of the fundus, for example, Plate I., Figs. 1 and 2.

The colour may be slightly deeper than this and duller
(Plate II., Fig. 4) ; or it may be a deep rich red, as is well seen
in Plate II., Fig. 6.

A disc that looks light by contrast is shown in Plate III.,
Fig. 5, and Plate IV., Fig. 8.

In exceptional cases the colour is a dull dirty red, as in
Plate VII., Figs. 18 and 19. The same colour is seen in part of
the disc in Plate VIII., Fig. 22, the central part of Plate V.,
Fig. 14, Plate VIII., Fig. 24. It will be noted, however, that
discs of this colour generally present other unusual features, so
that they can hardly be considered as typical.

The form and the extent of this intermediate portion of the
disc necessarily depend on the size, shape, and position of the
physiological cup. If there is no cup, the intermediate zone may
extend up to the centre of the disc (Plate II., Fig. 4, Plate

111., Fig. 7, Plate V., Fig. 12), or there may be a zone of con-
nective tissue forming a white, or pale, band round the central
vessels.

More commonly this part of the disc forms a broad belt
surrounding a central cup, which may be large or small (Plate

1., Figs. 1 and 2).

It is not unusual for the cup to open outwards, under these
circumstances the intermediate zone is displaced to the nasal side
(Plate XI., Fig. 30).

Differences in the level of the disc surface are important in
connection with inflammatory swelling of the head of the nerve,
but in the normal condition they hardly come under consideration,
for, unless special care be taken in the examination, the inter-

MARGIN OF DISC.

mediate zone always appears to be flush with the adjacent fundus.
But if a section of the eye be examined after its excision, the
disc will always be found to project slightly above the fundus.
And, even in the living eye, careful examination with the ophthal-
moscope will often afford indications that it is really raised.

Indeed, if it be borne in mind that the nerve fibres from all
parts of the retina crowd into the disc, and there become
continuous with the fibres of the optic nerve, and that the
apparent level of the fundus is not the surface of the retina, but
its pigment layer, it will be obvious that the surface of the disc
must project beyond the apparent level of the fundus.

It must be remembered that the appreciation of relief and
depression is largely due to experience, training, and unconscious
reasoning. So much is this the case that it is well known the
same figure may appear in relief or depressed according to the
incidence of light upon it, or even in accordance with the pre-
conception of the observer. In looking at the disc we see down
an unknown depth into its semi-transparent substance. The
colour is a blend of the capillary network, reflection from the
lamina, and the tissues of the nerve fibres. There being nothing
to fix the level, it is naturally referred to that of the adjacent
fundus. There are, however, often indications that the real level
is above this ; sometimes on the surface a fine gauzy piece of
connective tissue is visible, which, from the parallactic movement
it undergoes, is evidently in front of the fundus level. But the
most certain indication of the true level lies in the course of the
vessels. These can often be seen to spring forward from the centre
of the disc, and then to bend over in gentle curves to reach the
level of the retina (Plate I., Figs. 2 and 3, Plate X., Fig. 28).
Such vessels are always supported on the disc surface, which, being
transparent, is invisible. The cases in which a vascular loop
springs forward unsupported are too exceptional to be considered
in this connection, and moreover present a totally different and
unmistakable appearance. In commencing optic jieuritis, the

THE OPTIC DISC.

tissue of the disc becomes hazy, and then its true level is
easily discerned. Actual swelling of the disc occurs in this
condition, but in the early stage there may be turbidity without
swelling.

There remains for consideration the margin of the disc. Under
this term is included any part of the disc which lies beyond the
intermediate zone and a narrow belt of the fundus around the
disc. Strictly speaking, this cannot, of course, be included under
the term margin, but as the variations that it presents are
connected with alterations in the disc itself, the arrangement is
convenient.

The margin of the disc may be merely a line marking the
division between the intermediate zone of the disc and the fundus.
In such cases it corresponds to the edge of the choroidal opening.
Over this line, however, pass the nerve fibres from the retina to
the disc. These form a thick mass, so transparent that the fibres
themselves are invisible, but their presence considerably softens
the disc margin. This is seen from the fact that when the fibres
are atrophied, and their transparency thus increased, the disc
margin is seen as a hard sharp line, quite unlike its appearance
in health (compare Plate XXXII., Figs. 71 and 73, with those
which represent normal discs).

The nerve fibres are not evenly distributed over the margin,
but are most numerous above and below, and least numerous on
the temporal side In the latter situation the fibres are short,
and come from the macula, but the fibres from the parts
immediately above and below the macula curve round to reach
the upper and lower margins of the disc.

As already stated, the nerve fibres of the disc, as well as those
of the retina, are almost transparent, and, as a rule, invisible.
In young eyes, however, especially if the fundus is dark and the
refraction hypermetropic, a certain amount of light is reflected
from the surface of the fibres, so that they may be visible, although
transparent. It would seem that with advancing years some

MARGIN OF DISC.

change occurs in the tissues which renders them less reflecting ;
the nature of this change is not known, but the appearance
produced by light reflected from their surface is common in
children, rare in middle life, and unknown in old age.

The appearance referred to produces in the least marked cases
merely a light halo round the disc (Plate VI., Fig. 15, and Plate X.,
Fig. 29), while in the most marked, a gauzy film, which has a
fibrillar appearance, covers the disc margin. This is most con-
spicuous above and below, because the nerve fibres are here most
abundant (Plate I., Fig. 3, and Plate II., Figs. 4 and 6). It is also
frequently seen near the larger vessels, probably because the sur-
face is here a little raised. This condition must not be confounded
either with that known as opaque nerve fibres (Plate XII., Fig. 34,
and others), which will be described presently, or with blurring of
the disc margin, due to turbidity of the nerve fibres produced by
optic neuritis (Plate XXXI., Fig. 66). In the condition under
consideration there is no loss of transparency. The disc margin
can be seen through the gauze-like film that covers it. The
appearance is not fixed and constant like that produced by real
opacity, but changes with alterations in the direction of the
incident light, so that it may be most marked at different parts of
the margin in succession. This shiftiness and unreality in the
appearance make it difficult to depict it in a satisfactory manner,
for as soon as it is fixed in a drawing it has an unnatural hardness.
Although the natural appearance, however, cannot be accurately
reproduced, the figures referred to above, in which the attempt has
been made, come near the truth. Somewhat analogous appear-
ances are sometimes seen in other parts of the retina. They also
result from reflection from the surface of a transparent tissue,
which is not itself visible (Plate II., Fig. 5). The term reflex
phenomena is sufficiently descriptive of this class of ophthal-
moscopic appearance.

Another condition of disc and fundus occurs in association
with liypermetropia, and may resemble optic neuritis so closely
6

THE OPTIC DISC.

that it can be distinguished from it only by the fact that it
remains stationary. In these cases the disc margin is blurred,
white lines frequently accompany the vessels, and the latter are
unnaturally tortuous. I have myself only met with well-marked
examples of this hypermetropic disc in cases in which the
hypermetropia was of high degree, but Hubert Bristowe1 has
collected a considerable number of cases which seem to show that,
although this appearance only occurs in hypermetropic eyes, the
degree of error has no influence upon its frequency. Extreme
hypermetropia may be regarded as an arrest of development, and
it seems not unreasonable to look upon the tortuosity of the
vessels in these cases as connected in some way with a tardy
disappearance of the folded condition of the retina, which exists
in early foetal life.

The disc margin, if we adopt the definition laid down at the
commencement of this section, instead of being a mere line
separating the intermediate zone from the fundus, may be a band
of appreciable width encircling the intermediate zone like the tire
of a wheel (Plate I., Fig. 2, Plate V., Fig. 12, Plate XI., Fig. 31).
In the majority of such cases the band is obviously a part of the
disc, since it is marked off from the fundus by a much more defined
boundary than that which separates it from the remainder of the
disc. Its colour is much paler than the intermediate zone, but it
has not the brilliancy of exposed sclerotic.

This band is sometimes called the scleral ring — an obvious
misnomer, since it lies entirely within the disc. The real scleral
ring is never seen in its entirety except in pathological conditions.
(For examples, see Plate XXIV., Fig. 56, Plate XL VI I., Figs. 105,
106, and 107.)

The proper term for this band is the connective tissue ring, and
it is formed by a band of comparatively non -vascular tissue, which
is probably continuous with the pial sheath of the nerve. The

Ophth . Rev., London, vol. x., p. 321.

MARGIN OF DISC.

nerve fibres lie entirely within this ring, and are bound together
by it.

The connective tissue ring may be complete, or it may be
present at one part only, or it may be very wide at one part,
usually the lower, and narrow elsewhere. In the last case it
constitutes one variety of the condition to be presently described
under the name of congenital crescent of the disc (Plate VI.,
Fig. 15).

Occasionally this connective tissue ring is developed to such
a degree as almost to constitute a malformation of the disc
(Plate V., Fig. 14). The space available for the nerve fibres is then
encroached upon, and the fibres being consequently crowded
together, with less than the usual amount of connective tissue
between them, the intermediate zone has a peculiar dull greyish
colour, easily mistaken for atrophy. I have seen this grey colour
only in adult eyes. It seems probable such discs in early life
would resemble that shown in Plate V., Fig. 12.

In very exceptional instances it would seem that the con-
nective tissue ring not only encroaches on the intermediate zone,
but also on the choroid, so that the total area of the disc is
increased. Such cases may be looked upon as a variety of
coloboma of the disc (Plate VIII., Fig. 24).

The scleral ring can only be visible owing to the opening in
the choroid being larger than the space occupied by the optic
nerve, so that the sclerotic, or the junction of the sclerotic and
the upper end of the dural sheath of the nerve, is exposed.
It is sometimes difficult to be certain whether a ring should
be classed as scleral or as connective tissue, but a complete
scleral ring, evidently lying beyond the disc, is probably never
met with in health. It is not uncommon, however, for the sclera
to be exposed at one part of the circumference, usually the outer.
This is seen in Plate V., Fig. 13. The condition then resembles
that known as the myopic crescent. Indeed, it can only be
distinguished from it by the absence of myopia. Sometimes over

THE OPTIC DISC.

such an area only some of the layers of the choroid are absent,
and we may then have the appearance depicted in Plate VII.,
Figs. 20 and 21, and Plate XV., Fig. 40.

It is possible that certain cases of congenital crescent are
due to exposure of the sclerotic below the disc, although the
writer has never seen a case in which this explanation of the
appearance was not open to doubt.

The disc margin is usually, more or less pigmented. The
amount of pigment varies much. It may form a complete ring

Fig. 11. — Disc appearing to be oval from astigmatism.

round the disc. Most commonly it is defective in some situations,
while in others the pigment is abundant. In many cases, on the
fundus are broken lines of pigment parallel to the one which
coincides with the disc margin (Plate IV., Fig. 9, Plate VIII.,
Fig. 22). Less frequently a small amount of pigment lies within
the boundary on the disc itself (Plate II., Fig. 5). Exceptionally,
coarser masses of pigment are met with in this situation, which
may even cover a considerable part of the disc (Plate V., Fig. 11).

SHAPE OF THE DISC.

If the figures be examined it will be seen that, while there is
great variety in the distribution of this marginal pigment, it is
exceptional for it to be absent altogether.

The outline of the disc is usually nearly circular, although
minor irregularities, such as a slight flattening of some part of its
circumference, are very frequent. Oval discs are, however, by no
means uncommon, and then the vertical meridian is always the
longer (Plate II., Fig. 5). Fig. 12 represents rather an extreme
example of this, the ratio of the vertical to the horizontal meridian
being as five to three.

Fig. 12. — Oval disc.

The presence of astigmatism, however, may cause a disc to
appear oval when it is not so in reality, owing to its being more
magnified in one direction than in the other. In direct ophthal-
moscopic examination the enlargement is greatest in the meridian
of greatest refraction, but the actual effect produced (as is well
shown in Fig. 11, p. 44) depends less upon the difference in the
apparent length of the meridians of the disc than upon the contrast

THE OPTIC DISC.

between the sharp definition of all lines running parallel with
one principal meridian, and the indistinctness of those at right
angles to this.

Thus, Fig. 11 represents a case of astigmatism of 6 D. The
fundus is shown as it appeared when viewed through a spherical
lens, which corrected the horizontal meridian. All vertical lines
are seen with unnatural sharpness, so that the lateral edges of
the disc, and all vessels running in a vertical direction, stand out
boldty, while the upper and lower margins of the disc and all
horizontal vessels are blurred, or, at any rate, not conspicuous.
A very fair idea of the appearance can also be obtained by looking
at a drawing of a normal fundus through a cylindrical lens.

With the indirect method, the contrast between the vessels
is less marked, but the oval shape of the disc is readily seen.
When the object lens is held close to the eye, the longest diameter
corresponds to the meridian of least refraction (i.e., the reverse of
the appearance by the direct method), as the lens is withdrawn
from the eye, the meridian of greatest refraction elongates,
either actually, or relatively to the other meridian, so that the
disc becomes circular, and then elongated in the opposite
direction.1

In high myopia, also, the disc usually appears to be oval with
the long diameter vertical, owing to its being viewed obliquely
(Plate XXIII., Figs. 53 and 54).

1 For an admirable description and explanation of the changes produced by withdrawal of the
lens in the indirect method in the various conditions of refraction, the reader is referred to a paper
by M. Parent, Rec. d’ophth., Paris, 1881, p. 544.

CHAPTER III.

THE RETINAL VESSELS.

W e now return to the central artery and vein, which we left
at their point of entry into the eye, the artery having been just
reinforced from the plexus in the head of the nerve (Fig. 10, p. 31).

Owing to our habitually seeing the vessels magnified by the
dioptric system of the eye, we are apt to forget how small they
really are. The diameter of the largest probably does not exceed
one-hundredth of an inch.

Although we commonly speak of seeing the retinal vessels, it
must be borne in mind that what we see is not the vessel, but the
column of blood within it — a fact that can be easily demonstrated
by pressing on the globe with the finger during ophthalmoscopic
examination. The effect of this is to empty the vessels near the
disc, and it will then be seen that the empty portion of the vessels
will disappear from view, their walls being too transparent to be
visible. By careful focussing, the presence of the vessel wall can
occasionally be recognised by the existence of a fine line on each
side of the vessel, separated from the blood column by a very
narrow interval : this is most easily seen where one vessel crosses
another.

In the larger vessels the arterial blood is usually much brighter
than the venous, but in the smaller branches the distinction cannot
always be made, and the degree of difference varies in individual
cases. The arteries also appear brighter than the veins from the
presence of the streak of light which courses down the centre of
the vessel, and which is less marked in the veins.

The cause of the central light-streak has been much debated,
and the question cannot perhaps yet be considered finally settled.

THE RETINAL VESSELS.

Until recently it was generally held that it was due to reflection
from the anterior convex surface of the vessel or blood column.
Loring has, however, argued in favour of its being produced by a
reflection from the fundus behind the vessel, modified by the vessel
acting as a cylindrical lens. The objections to this view are so
cogent that it is difficult to see how it has obtained any supporters.
Thus, the reflex is not affected by the colour of the background ;
it exists on the disc as well as on other parts of the fundus ; and, if
Loring’s explanation were true, the streak would necessarily be red
and not white.

As to the distribution of the retinal vessels, we are met by
the initial difficulty that there is no arrangement sufficiently
common to be considered as the normal type. Perhaps the
most usual arrangement is for the central artery and vein
to emerge from the centre of the disc — each as a single vessel
— close to each other. In such cases the artery is, in the
great majority of cases, on the nasal side of the vein. Each
vessel then divides into an upper and a lower trunk, unless, as
is often the case, the division has already taken place in the
nerve. The upper and lower division soon bifurcate into an
inner and outer branch, so that we now have four named vessels,
the superior temporal and nasal, and the inferior temporal and
nasal. The temporal vessels are usually larger than the nasal, and
they curve round above and below the region of the macula, giving
off branches which pass towards the macula, but before they reach
it become too small to be visible. Besides the vessels just
described, separate small twigs usually emerge from different
parts of the disc surface, the most constant of these pass over
the temporal border of the disc and run in an almost horizontal

1 The reader who desires fuller information on this subject is referred to the following, among
other, papers: — Story, Ophth. Rev., London, vol. xi., p. 100; Jager, “ Ergebnisse der TJntersuch. mit
dem Augenspiegel, 1876;” Schneller, Arr.h.f. Ophth., Leipzig, bd. xxvi., ab. i.; Loring, “Text-boob
of Ophthalmology;” Dimmer, “Die Ophthalmoskopische Liclitreflexe der Netzlmut,” 1891; and
Bar. it. cl. Versnmml. Heidelberg ophth. Gesellsch., 1891.

NORMAL COURSE.

direction towards the macula, but they also appear to stop short
before they reach it.

The vessels are usually somewhat tortuous throughout their
course, but vary greatly in this respect. The veins may, broadly
speaking, be said to accompany the arteries ; that is to say, their
general direction is the same, and their branches usually correspond
to those of the arteries. But the curves made by the two sets of
vessels are often quite dissimilar, the veins being usually more
tortuous than the arteries. An artery and its corresponding vein
will frequently cross and recross each other, sometimes the one
and sometimes the other being superficial.

In some retinge the vessels proceed a long way from the disc
without bifurcating (Plate V., Fig. 11).

There is usually a relation between the number of vessels and
their size, but there are exceptions to this rule also, and in some
eyes the vessels are unusually numerous, while their size is little,
if at all, below the average.

The vessels as they pass from their point of origin over the
disc margin are usually seen to make gentle curves, having their
convexities forwards. As they lie on the surface of the disc
this indicates, as already pointed out, that the disc is slightly
convex.

The presence of a physiological cup modifies the course of the
vessels. When the cup is central, the main vessels usually emerge
from its floor, but instead of passing straight forwards they follow
the walls of the cup, climbing up them and curling over the edge
of the cup to reach the surface of the retina (Plate I., Figs. 1
and 2). If the cup is large and displaced laterally the vessels
are similarly displaced, as if they had been pushed aside by
the cup.

On the fundus the larger vessels lie in the fibre layer of the
retina. Only here and there do nerve fibres lie superficial to them.
Their presence is then indicated by a silvery gauzy reflex.

When, as is usually the case, the arteries and veins are equally
7

THE RETINAL VESSELS.

numerous, the veins are broader than the arteries in the ratio of
about four to three.

Vessels sometimes emerge from the margin of the disc, which,
when traced backwards into the nerve, appear to bend away in a
peripheral direction. It is probable that such come, not from the
central artery, but from the arterial circle round the head of the
nerve, or from one of the choroidal vessels. They, therefore, belong
more properly to the choroidal than to the retinal system, although
in their distribution they differ in no way from the branches derived
from the central artery.

Fig. 13. — Cilio-retinal vessel of large size.

These vessels, which are named cilio-retinal, are commonly
of small size and solitary, and emerge at the temporal border
(Plate XIX., Fig. 45). But occasionally vessels, both arteries and
veins, as large as primary branches of the central vessels are met
with, and they may emerge at any part of the margin (Plate VI.,
Fig. 15, and Fig. 13 above).

Usually it is only a matter of inference, from the direction of
the vessel, that it comes from the choroidal system, and it is

CILIO-RE TINA L VESSELS.

impossible to be certain that it has not sprung from the central
vessel in the substance of the optic nerve. Some authorities have
indeed doubted whether any of these vessels are really of ciliary
origin.1 Several cases are, however, on record, in which it has been
possible to trace the connection of such vessels with the choroidal
system, either with the microscope or with the ophthalmoscope.

Fig. 14. — Tortuosity of arteries and veins.

Thus, Nettleship has described and figured a microscopical
section of a disc in which a vessel of large size could be traced
from the sclerotic near the nerve entrance into the substance of
the disc.2 The case was one of optic neuritis, but although this

1 See Schnabel and Sachs, Arch. Oplitli. and Otol. N.Y., vol. xiv., p. 268.

2 Ophth. Hasp. Rep., London, vol. ix., p. 162.

THE 'RETINAL VESSELS.

might account for some increase in the size of the vessel, it could
hardly explain its presence as a new formation. Birnbacher1
describes a section of a perfectly healthy eye in Which a vessel,
believed to be an artery, as it lay in the choroid near the opening
for the optic nerve, gave off a branch, which passed towards the
papilla for a short distance, and then bending over the border of
the choroid, entered the superficial portion of* the nerve fibre layer
of the retina, and ran towards the macula.

Fig. 15. — Cork-screw twist of retinal vein.

Randall 2 gives a diagram showing the ophthalmoscopic appear-
ances in a case in which one of these vessels could be seen with the
ophthalmoscope joining a choroidal vessel 2 dd. from the disc-margin.
Similar conditions have been described by other observers.

The existence of these cilio-retinal vessels is not devoid of
practical importance, since occasionally when the main trunk of
the central artery has been occluded by an embolus, the presence
of one of them has permitted a portion of the retina to retain its

1 Arch. Ojphth. and Otol. , N.Y., vol. xvi., p. 32.

2 Trans. Am. Ophth. Soc., p. 513.

CILIO-RETINAL VESSELS.

function, and to remain unaltered in appearance. An instance of
this is shown in Plate XLI., Fig. 93. 1 2

Smaller twigs emerging from the outer margin of the disc, and
coursing towards the macula, are exceedingly common f their size
usually renders it impossible to be certain whether they are
arteries or veins. The larger cilio-retinal vessels generally appear
at other parts of the margin, and they not uncommonly bifurcate
close to their point of exit, as in Fig. 13, p. 50, and Plate VI.,

Fig. 16. — Projecting loops in retinal
vessels.

Fig. 17. — Projecting loops in retinal vessels.
(After Randall).

Fig. 15. The majority of cilio-retinal vessels are arteries, given
off from the circle of Haller ; when they are veins, they must be
offshoots of the choroidal vessels, since the circle of Haller consists
only of arteries.

A case has been recently published by Lawford,3 in

1 See also Benson, Ophth. Hosp. Rep., London, vol. x., p. 161, and Birnbacher, Centralbl. f.
prakt. Aucjenh., Leipzig, 1883, p. 207.

2 In a paper by Messrs. Lang and Barrett (Oplith. Hosp. Rep., London, vol. xii., p. 59) they are
said to occur in 16’7 per cent.; but the number of cases examined — 48 — is too small to establish
the frequency of the condition. The writer’s impression is that it is more common than this.

3 Trans. Ophtli. Soc., vol. xv., Plate VIII.

Fig. 19.- — Abnormalities in retinal veins. Fig. 20.— Abnormalities in retinal veins.

(After Werner.) (After Stephenson.)

emerged from the margin of the disc — a condition which occurs
normally in the felidoe and some other animals.

The retinal vessels never run even an approximately straight

TORTUOSITY OF VESSELS.

course, but their sinuosities present great variations in number,
character, and size. They are generally most numerous in the
veins, and a serpentine or wavy course, such as is shown in
Plate VII., Figs. 18 and 19, is not rare.

Both arteries and veins may be very tortuous, as in Fig. 14,
p. 51. We shall see later on that tortuosity of the retinal veins
is a symptom of optic neuritis, but in such cases they are also
distended, while the arteries are unaffected. Another point of
distinction is that physiological sinuosities lie (with occasional

Fig. 21. — Communicating branch between veins.
(After Stephenson).

Fig. 22. — Bifurcating vein.
(After Stephenson).

exceptions) in the plane of the retina, whereas many of the curves
produced by papillitis are perpendicular to it.

It seems that unusual tortuosity of the retinal vessels is more
frequently met with in hypermetropic than in other eyes. Hyper-
metropia, however, is so common a condition that too much stress
must not be laid upon the connection. But making due allowance for
this, tortuosity of vessels and hypermetropia are so frequently seen
together that the association cannot be accidental. Hypermetropia

THE RETINAL VESSELS.

is a condition of imperfect development ; may not tortuosity of
the retinal vessels be in some way connected with retarded
disappearance of the folded condition of the retina, which exists
at an earlier stage of development ?

Apart from general tortuosity of the retinal vessels,1 a single
vessel — usually a vein — may present a series of twists. These
usually lie in the plane of the retina, although isolated pro-

Fig. 23. — Bifurcating retinal veins.
(After Stephenson.)

Fig. 24. — Bifurcating retinal veins.
(After Randall).

jecting loops are occasionally seen on the larger vessels near the
disc.

Minor irregularities are exceedingly common. Thus an artery
and a vein may be twisted round each other like the strands of a
rope ; more often, as in Fig. 15, p. 52, it is the vein that is twisted
round the artery.

Occasionally, retinal veins as they proceed towards the disc
bifurcate (Figs. 18, 19, 22, 23, 24), or give off branches that

1 For good examples of tortuous retinal vessels the reader is referred to — Benson, Trans.
OjMh. Soc., vol. ii. p. 55 ; Nettleship, ib., p. 57 ; Mackenzie, il\, iv., p. 154.

TORTUOSITY OF VESSELS.

5 7

communicate with an adjoining vein (Figs. 20 and 21). Sometimes
one vein on the disc will take upon itself to receive most of the
others, and will go round a great part of the disc collecting them
(Fig. 20). In other cases a vein will bifurcate just before it
disappears into the disc, an artery passing through the fork
(Fig. 24).

A rarer anomaly is shown in Figs. 16 and 17, p. 53. Here
a vein forms a loop, each end of which disappears into the disc.
An analogous case is published by Lawford,1 in which one

Fig. 25. — Vessel projecting into vitreous from the disc.

extremity of the loop disappears at the centre of the disc, the
other at its margin.

An extreme instance of tortuosity of single veins is shown in
Plate XXI., Fig. 48. Others might be given, but as they occur
in almost infinite variety no useful purpose would be served by
doing so. Fig. 25, however, represents a condition which must be
exceedingly rare. A large vessel is seen to leave the centre of the

1 Trans. Ojphth. Soc., vol. xv., p. 195.

THE RETINAL VESSELS.

disc, to project into the vitreous at an angle of about 45° with
the apparent surface of the disc, and after proceeding about a disc
diameter, to divide into two branches, which twist round the
parent stem, and then return to the disc, in which they are lost.
The eye had normal vision.

Some who saw the case considered that the vessel was a
persistent hyaloid artery. Its size, direction, and bifurcation
are, however, all against this view, and I should look upon
it myself as an exaggerated example of a kink in a retinal

Fig. 26. — Remains of hyaloid artery.

vessel, and consider that the returning branches again emerge
as other vessels.

W. S. Little1 has published a somewhat similar case. Here,
however, the vessel did not return to the disc, but could be
traced on to the retina. It is difficult, therefore, to see on what
ground the author considers it to be an example of persistent
hyaloid artery.

The double loop in the vein shown in Fig. 16, p. 53, is probably

1 Trans. Am. OpJith. Soc., 1881.

PERSISTENT HYALOID.

of a similar nature. It will be seen that both extremities of the
loop disappear into the disc. The patient from whom the sketch
was made was suffering from slight optic neuritis associated with
albuminuria.

Persistence of the hyaloid artery as a blood-carrying vessel in
any great part of its course is one of the rarest congenital
abnormalities, although small portions of the vessel are not
infrequently seen. This vessel is a foetal structure, which passes
from the centre of the disc straight through the vitreous to the
posterior pole of the lens, where it breaks up into a plexus. A
retrogressive process occurs in the vessel, commencing at the lens,
and spreading backwards, so that at birth no vestige of it should
remain. The space in the vitreous, however, in which it lies — canal
of Cloquet or Stilling — persists throughout life, probably as a
lymph space, although its walls are too transparent to be visible
with the ophthalmoscope. Some congenital forms of posterior
polar cataract are, doubtless, connected with the remains of this
vessel. Instances have been recorded in which the hyaloid artery
has persisted in nearly its whole course as a blood-carrying vessel,
but more commonly it only forms a fine impervious thread, or an
empty tube. Fig. 26 shows a portion of the vessel persisting near
the disc, in the form of a truncated cul-de-sac, like the finger of
a glove, projecting into the vitreous, only its anterior extremity
is drawn in focus. It was of a light slate colour, and had a
thin gauzy appearance ; probably, therefore, it did not contain
blood.

Pulsation of the retinal vessels is a condition to which I
must refer, although for obvious reasons it cannot be depicted.
The retinal arteries are, of course, much below the size of
vessels in which pulsation occurs ; it is, therefore, never seen
in them, except as an abnormal condition, the essential feature
of which is that the resistance offered by the intraocular
pressure to the entry of blood is increased either actually, or
relatively to the propelling power of the heart. This may occur

THE RETINAL VESSELS.

either from increased intraocular pressure, as in glaucoma, or
from diminished propelling power, as in aortic regurgitation.
Arterial pulsation may also be produced artificially, by making
pressure on the globe during ophthalmoscopic examination, and
thus raising the intraocular tension. It is usually seen, not as
a rhythmical alteration in the calibre of the vessel, but as a sudden
disappearance and reappearance of a portion of the vessel on the
disc.

Arterial pulsation is also said to occur in exophthalmic goitre,
and is attributed to vasomotor paralysis. I have looked for this
symptom in all cases that have come under my notice, but hitherto
without success.

While arterial pulsation always indicates the presence of
abnormal conditions, it is otherwise with pulsation in the veins,
which is very commonly present in perfectly normal eyes, and is
due to purely physical causes within the eye itself. The veins are
readily compressible, but much more so in some eyes than in
others. At the height of the arterial pulse-wave there is a
momentary slight increase of the intraocular pressure ; this is
transmitted to the veins, and the blood in the part nearest the
centre of the disc is pressed out of the eye, so that a corresponding
part of the vessel disappears. We thus see one or more veins on
the disc alternately shortening and returning to their full length.
The pulsation is less sudden than that which occurs in the arteries,
and often resembles the to-and-fro action of a piston. It never
affects more than a short piece of the vein, and is most commonly
seen just at the point where a vessel curls over the edge of a
physiological cup, although it occurs also in other conditions.
For example, in Plate I., Fig. 1., the venous trunk, formed by the
union of the two lower veins, is just visible after passing beneath
the artery and before it dips into the cup. Such a vein would be
likely to show pulsation, the short piece referred to rhythmically
disappearing. Again in Plate I., Fig. 3, the lower vein would be
likely to exhibit the same phenomenon.

PULSATION IN RETINAL VEINS.

A slight increase in the intraocular pressure, whether occurring
spontaneously, or induced in the manner just described, will cause
venous pulsation, while a greater rise of pressure will produce
an arterial pulse. Venous pulsation can therefore hardly be said
to possess any diagnostic value, for it is present so frequently in
normal eyes, that in a case of suspected increase of tension it
would generally be impossible to prove that pulsation had not
always existed. Moreover, it is an undoubted fact that it may
be present at one time and not at another in a perfectly healthy
eye — a circumstance which is probably due to variations in the
action of the heart.

The explanation given above of the mechanism of venous
pulsation is not universally accepted, some authorities holding
that it is produced by the direct pressure of the artery on the vein
in the nerve or disc.

CHAPTER IV.

THE MACULA LUTEA.

We have now to turn our attention to the central part of the
fundus, which in men and apes presents a modified structure, and
possesses a highly exalted function. This differentiation of the
centre from the remainder of the fundus marks the highest stage
reached in the evolution of the eye, and is no doubt an essential
factor in binocular vision.

This central region has been called the yellow spot (macula
lutea) or, more briefly, the macula. The name is derived
from a transient discoloration which takes place in this area
after death, and has no connection with its ophthalmoscopic
appearance. In the centre of the macula is sometimes to be
seen a minute depression, which is usually called the fovea
centralis.

The macula presents no sharply defined boundary either with
the microscope or with the ophthalmoscope. Automatically
it may be defined as the region in which the bacillary layer
is represented by cones only. With the ophthalmoscope it
sometimes appears to be surrounded by a silvery halo or
reflex ring. Either of these limitations will include an oval
area, the major axis of which is transverse and about the same
length as the diameter of the disc. Its centre is situated
about a disc and a half from the outer margin of the disc, and
a little below the horizontal meridian.

Until recently the macula has usually been described as
lying on the same level as the rest of the retina, but presenting
near its centre a depression which was called the fovea

ANATOMY.

centralis. Recent investigations
by Dimmer 1 have shown that
the depression commences at the
border of the macula, and shelves
down gradually to the centre,
where sometimes there is another,
smaller, depression. This small
and occasional depression cor-
responds with the white spot
seen with the ophthalmoscope,
and hitherto called the fovea
centralis ; Dimmer would call
this the foveola, using the
term fovea as synonymous with
macula.

If we accept these views, the
ophthalmoscopic appearances are
brought into harmony with the
anatomical structure. Thus, the
reflex ring is at once explained
by light being reflected from the
slightly raised convex edge of the
depression. The thinning of the
retina within the area explains
the colour of the macula. In
pigmented eyes this is often dark
from the pigment of the choroid
showing through, while in lighter
eyes, the capillary layer of the
choroid gives it a richer red.

Of the anatomical modifica-
tions of this part, the most

1 “ Beitrage zur Anatomie und Physiologie
der Macula lutea des Menschen,” 1894.

Fig. 27. — Section of retina in macular region. (After Dimmer.)

THE MACULA LUTEA.

characteristic is the entire disappearance of the rods from the
bacillary layer, so that the cones are numerous, and in contact
with one another. As the centre is approached they increase
in length.

Round the borders of the macula most of the layers become
somewhat increased in thickness, and they then gradually thin
down. This is especially noticeable in the layer of nerve cells.
Around the macula, the cells are ten deep, while at the fovea
there is but a single layer.

According to Golding Bird and Schafer,1 there is a depression
in the external limiting membrane, corresponding in position to
the fovea (Fig. 28).

An anatomical peculiarity of this region, which has a

considerable influence upon the
ophthalmoscopic appearance
under certain conditions, is
the oblique direction assumed
by the fibrillar elements,
namely, the cone-fibres, and
the fibres of Muller. Instead
of traversing the retinal layers
in a perpendicular direction,
as in other parts, they become
more and more oblique as the
centre is approached. The
result of this is that, instead of seeing merely the inner
extremities of Muller's fibres, the whole length of the fibres
is exposed, and, if opaque, they appear as lines radiating
from the fovea. Indications of this arrangement of the fibres can
sometimes be seen faintly indicated in normal eyes (Plate III.,
Fig. 8) ; it is often conspicuous in pathological conditions
(Plate XXXVII., Fig. 84).

The appearance just referred to is not identical with that

Fig. 28. — Section through the macula. (After
Golding Bird and Schafer.

1 lnternat. Monatschr. f. Anat. u. Physiol., Leipzig, 1895, hd. xii., heft. 1.

MACULAR REFLEX.

described by Bristowe,1 in which there were bright radiating
lines, “ suggesting a resemblance to the petals of a sunflower/'
This latter phenomenon is evidently a reflex appearance,
analogous to the watered-silk streaking that is seen in other
parts of the retina, and, as in that condition, the streaks appear
to lie on a plane anterior to the retina. The striation, on the
other hand, which is produced by the retinal fibres, lies in the
retina.

The ophthalmoscopic appearance of the yellow spot varies
much. In light fundi it is seldom conspicuous, and its position
may only be recognisable by a slight deepening of the colour of
the fundus (Plate III., Fig. 7), or by an absence of visible blood
vessels. In these light fundi the fovea centralis is often not
noticeable, while in moderately dark fundi, on the other hand, both
yellow spot and fovea are usually conspicuous. The former as a
dark area, sometimes showing fine pigment stippling (Plate II.,
Figs. 4 and 6) ; the fovea as a rounded white dot in its centre
(Plate II., Fig. 5). In very dark eyes the macula is often of a still
deeper hue than the rest of the fundus (Plate X., Fig. 29 ; Plate
XLII, Fig. 95).

As already stated, in some eyes which are perfectly normal,
faint indications can be seen of strise radiating from the fovea
(Plate III., Fig. 8). This radiating or star-like appearance is
doubtless due to the alteration in the direction of the fibres at
this part, already described. In normal eyes it is seldom to be
seen, and is never conspicuous, but in some morbid conditions
it is very marked (Plate XXX Y., Fig. 78 ; and Plate XXXVII.,
Fig 84).

A reflex appearance at the macula, which is common in
young subjects, is that of a delicate white or silvery ring of oval
shape, corresponding in size with the boundary of the macula,
and seeming to float just in front of the retina. This reflex ring
or halo is seen best with a concave mirror and by the direct

1 Ophth. Rev., London, vol. x., p. 322.

THE MACULA LUTE A.

method, but it can also be seen by the indirect method. Some-
times it is visible in its entirety ; more commonly one or other
part of it comes into view according to the position of the mirror.
It is impossible to depict it without making it appear more sub-
stantial than the reality. The macular halo is doubtless due to
thickening of some of the layers of the retina at the borders of
the yellow spot, a slight convexity being thus produced, which
reflects the light.

The smaller central depression, when it exists, also has its
reflex appearances. The most common of these is a minute

crescent of light, embracing
about half the circumference
of the depression, and travel-
ling round it as the mirror
is moved. Another is a short
beam of light appearing to
project from the bottom of the
depression a short distance
into the vitreous. This has
received the name of the
policeman’s lantern reflex,
which, if rather fanciful, is
yet sufficiently descriptive.
This appearance was first de-
scribed, I believe, by Marcus
Gunn,1 who considered that it was usually associated with
myopia ; it is, however, certainly met with in all states of
refraction.

Ophthalmoscopic examination of the macula without the
previous employment of a mydriatic is often difficult, because the
pupil contracts strongly when the light falls on this region,
and also because the corneal reflection of the mirror lies in
the line of sight. Hence many observers are less familiar with

1 Trans. Ophth. Soc., vol. viii., p. 173, and Ophtli. Hosp. Rep., London, vol. xi., p. 348.

Fig. 29. — Entoptic appearance of vessels at
macula. (Graefe u. Saemisch.)

DOTS AT MACULA.

the physiological variations of this part than they are with those
of the optic disc. Consequently, when an unexplained amblyopia
leads to a thorough examination, changes at the macula are
apt to be diagnosed on rather insufficient evidence.

Reference has been made to the absence of visible vessels
within the macula. Their invisibility is, however, due only to
their small size. With the microscope they can be traced to the
edge of the fovea.

Their presence can also be shown by what is known as the
entoptic method, in which shadows of the vessels are thrown
upon the retina, and are projected by the subject of the experiment
as if they were the images of external objects. The experiment is
performed in the following manner : — A white cloud is looked at
through a pinhole in an opaque diaphragm. The latter is then
rapidly moved about, care being taken to keep the aperture
within the area of the pupil. The visual field at first appears
of an uniform grey colour ; it is soon seen, however, to be crossed
by a network of darker lines, which branch and anastomose, thus
forming a fine plexus (Fig. 29).

White or yellowish dots are occasionally met with at the
macula in eyes which appear to be healthy. Some of these are
conspicuous notwithstanding their minute size, owing to the
hard, sharp appearance which they present. Others are seen
with difficulty, and only when the light is feeble or strikes them
obliquely. The latter are identical with those described by Mr.
Gunn under the name of “ Crick ” dots. They will be described
more fully later on (Plate III., Fig. 8 ; Plate IV., Figs. 9 and 10 ;
Plate XI., Fig. 30.

CHAPTER V.

DEVELOPMENTAL IRREGULARITIES.

So far we have been dealing with conditions which in no way
impair the function of the eye, and which may therefore be
termed physiological. We must now turn our attention to
those which are due to an arrest of, or to an irregularity in,
the process of development. These may be said to lie on the
borderland between physiological and pathological conditions ;
for, on the one hand, they are congenital and stationary ; on the
other, they usually interfere to some extent with function.

COLOBOMA OF THE CHOROID.

Coloboma of the choroid is one of the most conspicuous of
these conditions. Its morbid anatomy can only be understood
by bearing in mind the principal stages in the process of
development of the eye.

The optic nerves and retinm are formed from the neural
epiblast, and are at first represented merely by two hollow protru-
sions from the anterior cerebral vesicle. Each of these protrusions
subsequently becomes differentiated into a tubular stem — the
optic stalk, and a more globular extremity — the primary optic
vesicle. At this stage the optic stalk contains no nerve fibres.

The vitreous body and the blood vessels of the optic nerve
and retina are developed, on the other hand, from the mesoblast,
a process of which enters the globe below, and in so doing pushes
the wall of the primary optic vesicle in front of it.

The wall of the primary optic vesicle thus becomes invaginated,
and doubled on itself, and its cavity obliterated. This pushing

COLOBOMA OF CHOROID.

in of the mesoblastic process, while obliterating the primary optic
vesicle, produces a new cavity — the so-called secondary optic
vesicle. This contains the process of mesoblast, which subse-
quently becomes the vitreous. It is bounded by the now redupli-
cated wall of the primary vesicle, which afterwards becomes the
retina. The retina, in the early stages of its development, presents
numerous folds, and the entrance of nerve stalk is much larger
in proportion to the rest of the organ than is the optic disc
into which it develops. The wall of the secondary optic vesicle
is necessarily imperfect below, where there is a gap to permit
the entry of the process of mesoblast. This gap, which may
be called the foetal cleft, extends anteriorly to the lenticular
depression in the cutaneous epiblast, and posteriorly to the optic
nerve stalk.

The portion of mesoblast that lies outside the cleft eventually
surrounds the eye and becomes differentiated into choroid and
sclerotic. That inside the cleft, besides developing into vitreous,
carries a number of blood vessels into the interior of the globe.
The greater number of these disappear early in foetal life, but
others are pushed into the optic nerve stem — along the wall of
which nerve fibres are now growing — and become the central
vessels of the retina. Up to a comparatively late period another
vessel also persists — the hyaloid artery. This extends from the
centre of the optic nerve across the cavity to the posterior surface
of the lens, where it breaks up to form a plexus.

In the normal course of development the mesoblastic process
should disappear, and the cleft close, so that at birth no vestige
of either should be visible. According to most authorities1 the
closure of the cleft commences posteriorly and extends forwards.
It should be completed by the end of the second month. The
closure may be arrested or delayed at any stage, so that a gap
may remain in the ocular tunics extending from the ciliary body
to the disc, or stopping short at any distance from the latter.

1 Bock, “Die angeborenen Kolobome,” etc., 1893.

DEVELOPMENTAL LRREG ULARLTLES.

Associated with this is usually a defect in the corresponding part
of the iris. This coloboma of the iris looks like a neatly performed
iridectomy. It is not immediately due to non-closure of the foetal
cleft, for the iris does not exist at the time at which this should
take place, but is a later outgrowth from the choroid. In the
normal course of development the iris presents no cleft at any stage.

The condition produced by non-closure of the foetal cleft is
usually spoken of as coloboma of the choroid. Its ophthalmo-
scopic appearance is shown in Plate IX., Figs. 26 and 27. If the
above account just given of the development of the eye is correct,
it would be more accurate to look upon the condition as primarily
a coloboma of the retina. It would seem, however, that the
patency of the cleft so modifies the conditions of development that
all the tunics are imperfectly formed.

As to the condition of the retina, its pigment layer is always
completely absent over the area concerned, while at the margins
of the gap pigment is frequently heaped up. The nervous elements
appear to be absent, if we may judge from the fact that the visual
field always shows a gap corresponding to the coloboma. It is
true that in a few eyes which have been examined microscopically,
some tissue has been discovered which was believed to be retinal,1
but only in small amount, and very imperfectly developed. The
retinal vessels may, however, be present and course over the
coloboma as in the figures. This is to be explained by the fact
that they are a late development from the mesoblastic process, as
explained above.

The choroid may be said to be practically absent, since neither
pigment nor blood vessels exist, and the normal choroid is mainly
made up of these.

The sclerotic, also, is modified, so that it yields to the intraocular
pressure and becomes bulged outwards. This is seen to a slight
degree in Plate IX., Fig. 26, but sometimes the protrusion is so
extreme that a cyst is formed which may be larger than the eye

1 Hess, Arch, f Ophth., Leipzig, bd. xxxvi., p. 137; Bock, loc. cit.

COLOBOMA OF CHOROID.

itself, which in such cases is always smaller than normal. In this
circumstance we have an explanation of some of those rare cases of
supposed absence of the eye (anophthalmos) associated with the
presence of a cyst in the lower eyelid. But, although such an
extreme condition is rare, some degree of microphthalmos is
common in coloboma.

When a coloboma reaches nearly to the disc (as in Plate IX.,
Fig. 26), the latter appears shortened in its vertical diameter ;
this is probably due mainly to the fact that the bulging of
the sclerotic tilts the disc forwards, and its vertical diameter is
thus foreshortened. If the disc is involved in the coloboma, it
may be unrecognisable except as the meeting point of the vessels,
or it may present a deep depression much larger than the normal
disc. The subject of coloboma of the disc will, however, be
considered later, as well as the possible connection between
congenital crescent of the disc and delayed closure of the cleft.

Delay in the closure of the cleft is probably due to persistence
of the mesoblastic process beyond the normal time. This persistence
may affect one part only, when a partial coloboma will be produced.
This appears to have been the case in the left eye of the patient
whose right eye is depicted in Plate IX., Fig. 27, for although the
fundus presented a normal appearance near the disc and towards the
periphery, there was an irregular area of exposed sclerotic about
2 dd. below the disc, which roughly resembled the upper portion
of the coloboma depicted in the figure.

Coloboma of the iris is not unfrequently present without any
defect in the choroid. Even then, however, the gap is usually
directed downwards, although exceptional cases are met with in
which it occupies other situations.

Coloboma of the choroid, on the other hand, seldom exists
without a corresponding defect in the iris ; such cases have,
however, been recorded.1

1 F. J. Becker, Arch. f. Ophth., Leipzig, bd. xxii., p. 221 ; Talko, Klin. Monatshl. /. Augenh.,
Stuttgart, 1875, p. 215 ; Benson, Dublin Journ. Med. Sc., 1882 ; Hoffmann, “ Inaug. Dissert.,” 1871.

DEVELOPMENTAL IRREGULARITIES.

It is generally held that coloboma of the choroid, from arrested
development, can occur only in the downward direction. It is true
that defects in other directions have been described, but as these
were associated neither with coloboma of the iris, nor with
microphthalmos, they have usually been attributed to destruction
of the choroid by inflammation, and not to its non-development.

Recently, however, the writer saw a case 1 in which a coloboma
of the choroid on the temporal side co-existed with coloboma of
the iris similarly situated, and with microphthalmos. The patient
was a girl aged 11. The diameter of the right cornea measured
only 9 mm., and the whole eye was evidently small. There was a
coloboma of the iris on the temporal side, involving about one-eighth
of its circumference. The margin of the lens was visible through
this, and presented no abnormality. The coloboma of the choroid
extended from the temporal periphery to a point about ~ from the
temporal side of the macula, where it ended in a rounded border.
There was nothing abnormal either in the appearance of the optic
disc, or in the direction of the principal vessels.

Some writers have attributed coloboma to an inflammatory
process occurring during intra-uterine life. It must be admitted
that a case like the above gives some colour to such a view, but
the almost constant position of the defect downwards is strong
evidence in favour of the foetal cleft being in some way concerned
in its production.

Opaque Nerve Fibres.

A conspicuous congenital abnormality of the disc is that
presented by the condition known as opaque nerve fibres. We
have seen that at the level of the lamina cribrosa the fibres of the
optic nerve change their character ; for, whereas behind the
lamina they consist of axis cylinders encased in medullary sheaths ;
in the fibre layer of the retina there are axis cylinders only. It

1 Trans. Ophth. Soc., vol. xiii., p. 144.

OPAQUE NERVE FIBRES.

occasionally happens, however, that a few fibres on the retina
are also encased in medullary sheaths like those in the optic nerve.
We then have such an appearance as is represented in Plate XII.,
Figs. 34 and 35, and Plate XIV., Fig. 38. It will be noticed in all
these that the disc itself presents nothing abnormal. Evidently,
therefore, the affected fibres have not retained their medullary
sheaths continuously from the optic nerve, but have thrown them
off before traversing the lamina, and again resumed them. This
was found to have actually occurred in some cases, which were
examined both ophthalmoscopically during life, and microscopically
after death.1

The ophthalmoscopic appearance will vary with the number
and position of the affected fibres, but there are certain features
common to all cases. The patch is of a very brilliant white colour,
quite unlike an inflammatory exudation, or a patch of exposed
sclerotic. Its surface can usually be seen to be fibrillated. When,
as sometimes occurs, it appears to be rough, or almost crystalline,
its fibrillar nature is clearly indicated at the edge of the patch,
where it merges into normal fundus, by the fine brush-like pro-
cesses into which it splits.

The retinal blood vessels are usually wholly or partially
embedded among the opaque fibres.

The white area is usually in contact with the margin of the
disc, and extends on to the retina about a disc diameter.
Occasionally there is a clear space between the patch and the
disc as in one of the tufts in Plate XIV., Fig. 38. It is rare
for the opaque nerve fibres to lie at any distance from the disc,
but a case is recorded by Recklinghausen,2 in which a space of
4 mm., or about two disc diameters, intervened.

In extreme cases, the disc itself is involved (as in Plate XIII.,
Figs. 36 and 37, and Plate XIV., Fig. 39), so that a great part,

1 Schmidt-Rimpler, Klin. Monatsbl. f. Augerih., Stuttgart, 1874, p. 186 ; Manz, Arcli.f. Augenh.,
Wiesb., bd. xxix., p. 220.

2 VirrJww’s Arclriv, bd. xxx., p. 375 ; and Usher, Oplitlx. Rev., London, vol. xv., p. 1.

DEVELOPMENTAL LRREG ULARLTLES.

or even the whole, of the disc may be hidden. The part that
remains visible is commonly of a dark dull colour, similar to that
which is met with in extreme examples of congenital crescent
(compare Plate VIII., Fig. 22, with Plate XIII., Figs. 36 and 37,
and Plate XIV., Fig. 39). No doubt this colour is partly due to
contrast with the adjacent white patch, but it is probably mainly
produced by the crowding together of the remaining nerve fibres,
and the diminution in the quantity of interstitial tissue, caused by
the disproportionate amount of space occupied by the coarser
opaque fibres. In these cases where the disc is involved there
can be little doubt that the opaque fibres are continued through
the lamina ; indeed, this was proved to be the case in an instance
recorded by W. Manz.1

The conducting power of the affected fibres is not impaired, and
vision therefore is not appreciably affected. At the same time
the opacity of the fibres prevents images being formed on the
sentient layer beneath them, and the size of the blind-spot is
consequently increased to an extent corresponding to the patch
of opaque nerve fibres. Usually this increase is too slight to be
observed, but in the case from which Fig. 39 was taken it was
quite perceptible with the perimeter.

Microscopical examination of eyes in which the presence of
opaque nerve fibres has been discovered during life, has not often
been possible. But particulars of a few such cases are given in
the papers just quoted.2 The affected fibres in all presented
varicose swellings, which were connected with the axis cylinders ;
but the explanation of this association is not obvious.

A condition that bears some resemblance to opaque nerve
fibres is the striated appearance of the disc margin (Plate I.,
Fig. 3, and Plate II., Fig. 4), already described as being not
infrequently seen in young eyes, especially if the fundus is rather
dark. In these cases, however, there is not the brilliancy of
opaque nerve fibres, and the striation, instead of being definitely

1 Loc. cit.

2 Loc. cit.

CONGENITAL CRESCENT OF THE DISC.

localised at one part of the disc, shifts its position according to the
direction of the incident light.

A case has been recorded 1 in which a patch of opaque nerve
fibres disappeared when the optic disc became atrophied. This
cannot be a constant result, as the writer has seen the conditions
of opaque nerve fibres and optic atrophy in association.

It is not uncommon to see masses of connective tissue on the
disc. In the slighter cases little white threads, so fine as to be
easily overlooked, lie in front of the apparent level of the disc, and
may indicate the real position of the summit of the nerve head ;
they may, however, project a short distance into the vitreous, and
undergo tremulous motion after the eye has been quickly moved.
It is difficult to depict such fine opacities in a satisfactory manner.
In more marked instances a well-defined white mass is seen over
the central vessels, often sending out processes which accompany
the branches of the arteries a short distance ; in such cases the
connective tissue may either form a dense white mass, or a light
feathery fluff over a part of the disc (Plate XII., Figs. 32 and 33).

A somewhat analogous appearance, which is rare, is a white, or
grey ring about the diameter of the disc, and lying well in front
of it ; it probably has some connection with the canal of Cloquet.

Indeed, it is not improbable that many of the finer gauzy
shreds which lie on a plane anterior to the disc may be remnants
of the hyaloid artery.

Congenital Crescent of the Disc.

I have chosen the above title for this condition in preference
to that of Coloboma of the Disc, which is sometimes applied to it,
both because it sufficiently describes the ophthalmoscopic appear-
ance, without committing us to any theory as to its pathology,
and also because there is another condition of the disc to which
the term coloboma can be more appropriately applied.

1 Wagenmann, Arch./. Ojphth., Leipzig, bd. xl., p. 256.

DE VELOPMENTAL IRREG U LARI TIES.

These congenital crescents are exceedingly common, at any
rate in a slight form. They consist of a crescentic area of paler
colour than the rest of the disc, situated, with a few exceptions,
directly downwards, or downwards with a slight obliquity.

The contrast between the colour of the disc and that of the
crescent is generally better seen by the indirect than by the direct
examination. The boundary line between the crescent and the
rest of the disc usually forms a segment of a larger circle than
the remainder of the disc margin, and is sometimes a straight
line. The disc and crescent together usually form a figure that is
nearly circular or oval ; in the latter case, the direction of the
axes corresponds to the astigmatism, which is very often
present. This is seen in Plate VII., Figs. 18 and 19, in which
there was astigmatism of 40 B. It will be noticed that while
the coloured portion of the disc is round, it, and the crescent
together, form an oval, the long diameter of which corresponds
to the meridian of greatest refraction.

In many instances visual acuity is subnormal after the refraction
has been corrected.

A slight degree of this anomaly, as shown in Plate VI., Fig. 15,
may be taken as an example, while Plate VIII., Fig. 22, represents
a very pronounced form of it. The other drawings show inter-
mediate varieties (Plate VI., Figs. 16 and 17 ; Plate VII., Figs.
18 and 19).

It will be seen that the limbs of the crescent pass round the
disc to a varying extent, and frequently become prolonged into
a narrow band of the same colour which encircles the remainder
of its circumference. Fuchs, in his admirable paper1 on this
subject, speaks of this as the scleral ring ; it is possible that in
some cases the limbs of the crescent merge into the scleral ring,
but in all the cases I have myself seen it has seemed to me that
they blended with the connective tissue ring, and that both the
crescent and this ring formed parts of the disc, and did not lie

1 Arch. f. Oplith ., Leipzig, bd. xxviii., ab. 1, p. 139.

CONGENITAL CRESCENT OE THE DISC.

beyond it. The same author also says that the area of the crescent
is generally slightly depressed, but admits that the uniform
appearance of its surface renders accurate measurement of its
level difficult. I have not been able to satisfy myself as to the
existence of this depression in any uncomplicated case. Nor does
it seem to me that the abnormal arrangement of the vessels, of
which he speaks, is at all common. This consists in the larger
retinal vessels passing first to the inner side of the disc, and
afterwards bending round to be distributed over the outer
part of the fundus.

The physiological cup is very often absent in these cases
(Plate VII., Figs. 18 and 19). When present, it appears always to
open towards the crescent ; that is to say, the edge furthest from
the crescent is steep, while on the side towards the crescent the
floor of the cup slopes up gradually ; the vessels either creep
round close under, or pierce the steep edge.

The colour of the disc in well-marked cases generally differs
from the normal, in being darker (Figs. 18 and 19) ; this is
not merely the effect of contrast with the white crescent,
although, doubtless, that has some influence. The disc, also, often
has the appearance of being composed of a more transparent
although darker substance than usual, so that the vessels instead
of disappearing into it suddenly, pass out of sight gradually as
if they were sinking into a semi-transparent substance. This is
well seen in Plate VIII., Fig. 22.

Congenital crescent has been explained as due to a kind of
partial deficiency in the substance of the disc, a gap existing so
that one sees down a short distance into the scleral sheath. There
is seldom, however, sufficient difference in level between the
disc and the crescent to allow us to accept this explanation.
Another view is that there has been a non-closure of the foetal
cleft at the disc, so that here we have exposed the sclerotic or the
junction of the dural sheath and sclerotic ; if this explanation be
true, the crescent must lie beyond the disc, its limbs being

78 DEVELOPMENTAL IRREGULARITIES.

continuous with the scleral ring. Analogous crescents of very
small size are met with at the outer margin of the disc, as in
Plate V., Fig. 13, and no doubt they may occur below, but in
all well-marked cases of crescent in this situation, they have seemed
to me to form a part of the disc. When, as in Plate VII., Figs.
20 and 21, the crescent is partially covered by choroidal tissue,
it must be considered to lie beyond the disc, but these seem to
differ materially from the ordinary form of congenital crescent.
Congenital crescents, in the opinion of the writer, are due to

Fig. 31. — Diagram of hypothetical condition of
lamina cribrosa in congenital crescent ; much
connective tissue below, little elsewhere.

an uneven distribution of the tissue of the lamina cribrosa. Fig.

30 shows diagramatically the normal arrangement of this ; if now
we suppose the tissue of the lamina, while maintaining its proper
proportion to the nerve tissue, to be massed at the lower part
instead of being evenly distributed through the nerve (Fig. 31)
we have an explanation of the ophthalmoscopic appearances.

According to this explanation, the colour of the disc is due to

Fig. 30. — Diagram of lamina cribrosa ; connective
tissue uniformly distributed.

COLOBOMA OF THE DISC.

crowding together of the nerve fibres, with very little tissue
between them. We saw a similar effect produced in an analogous
manner in cases of opaque nerve fibres.

A variety of congenital crescent not often seen is shown in
Plate VIII., Fig. 23. In this the crescent, which is of large size,
is situated above the disc. It is interesting to note, that notwith-
standing the unusual position of the crescent, the physiological
cup is still directed towards it. The writer has seen several
examples of small crescents situated above. In one of these, the
disc in the other eye presented a crescent above and below.

A disc such as that shown in Plate VIII., Fig. 24, presents
some points of analogy with congenital crescent. But here the
connective tissue forms a wide ring, and the remainder of the disc
is depressed. It would, therefore, be probably more correct to look
upon this as a partial coloboma of the disc.

COLOBOMA OF THE DlSC.

Coloboma of the disc may occur in various degrees, and present
very different ophthalmoscopic appearances.

As already stated, coloboma of the choroid may extend to, and
involve the disc, which in some cases may be seen lying in the
coloboma, but not much altered, except that its surface has a
downward inclination, which makes it appear oval with its long
diameter transverse. In other cases — and these are the more
numerous — the upper margin of the disc is sharply defined, or
overhanging, while the lower merges into the coloboma without
any distinct line of demarcation.

Coloboma of the disc may, however, be present without any
gap in the choroid. In well-marked cases, the disc area is much
increased in size, and presents a large and deep depression. This
may be funnel-shaped, so that no floor is visible, or there may be
a glistening bluish-white floor, the colour of exposed sclerotic, or,
again, the depression may be filled up by a semi-transparent

BE VELOPMENTAL IRREG ULARITIES.

substance, which can be penetrated with the light from the
ophthalmoscope to an uncertain depth.

Good examples of this condition are seen in Figs. 32 and 33,
which represent respectively the right and left eye of the same
patient. The disc area in the right eye is about three-and-a-half
times the normal diameter. Above, the vessels dip down gradually
into the deep depression, and disappear from view. Below, they

Fig. 32. — RE. Coloboma of optic disc. (After Benson, Dublin Journ. Med. Sc., 1882.)

curve abruptly over the upper edge of the crescent, which is on
the same level as the fundus, to reach a lower depth ; they then
run over a level terrace, and disappear over its edge into the
deepest depression.

The left eye (Fig. 33) shows a somewhat similar condition, but
in a much less marked degree. It is to be noted that in both eyes
there are indications of imperfect closure of the choroidal cleft.

COLOBOMA OF THE DISC.

Colobonm of the disc doubtless depends on a non-closure of the
cleft that exists in early foetal life at the lower part of the nerve.
Probably, also, the nerve sheath retains to some extent its
embryonic condition of a hollow tube, with the nerve fibres spread
out on its inner surface, instead of being collected into a compact
cord.

A condition analogous to Plate VII., Fig. 21, is shown in

Fig 33. — LE. Coloboma of optic disc. (After Benson, loc. cit.)

Plate VIII., Fig. 25, but the hollow involves less of the disc area,
and is filled up by a semi-transparent substance. The vessels
emerge near the centre, and all, except those which pass upwards,
disappear gradually into the depression ; below is a crescentic
uncupped area like a congenital crescent, over the edge of which
the lower vessels curve abruptly. Plate VIII., Fig. 24, probably
represents an analogous, but less marked, condition.

In some cases of partial coloboma the depression occupies but
ll

DEVELOPMENTAL LRREGULARLTLES.

a small portion of the disc. It is situated near its border, as
in a case published by Mr. Randall, the drawing of which
is reproduced in Fig. 34. The disc had twice the normal
diameter, and presented at its upper part a narrow crescentic
portion of approximately normal colour on the same level as the
fundus. Of the upper vessels some emerge through this, others
come round its lower edge. The lower vessels come out from
under the edge of this crescent, and one, larger than the others,
again disappears into the depression at the lower part of the
disc. The greater part of the disc was on a level 6 D. lower than

Fig. 34. — Coloboma of disc. (After Randall, loc. cit.)

the upper part, and was divided into two parts, the upper having
a greenish opalescent colour, like exposing sclerotic, the lower
resembling a congenital crescent. In the lower and inner part
of this, close to the disc margin, was the circular pit already
referred to. This appeared to be 4 D. deeper. Into its upper
part dipped the large vessel already mentioned, while from its
lower margin three vessels emerged.

Circular or oval depressions like that just described are
occasionally seen in discs which present no other abnormality.
They are generally of grey colour, and have an ill-defined

COLOBOMA OF THE DISC.

appearance of depths, owing to the impossibility of seeing the
floor clearly. This difficulty may arise from the small amount
of light that is reflected from the bottom of a deeper and narrow
depression, or from a partial filling up by a substance which is
imperfectly transparent.

A case of this kind with normal vision has been recorded by
Marcus Gunn.1 In this there was a small patch of choroidal
atrophy close to the disc margin on the lower and inner side. In
the outer part of the disc was a funnel-like excavation, which

Fig. 35. — Partial defect in disc.

passed so deeply into its substance that the floor could not be
seen by the direct method. The outer edge of the disc overhung
the depression. When this is the case the area of the depression
may vary with the position of the observer, owing to the parallactic
displacement of the overlapping edge.

Mr. Stephenson has been good enough to furnish me with a
diagram (Fig. 34) of a similar case seen by him. The patient was
a boy of ten, with normal vision. In the left eye was a large

1 Trans. Ojphth. Soc., vol. vi., p. 375.

DEVELOPMENTAL IRREG ULARLTIES.

circular cup, with stippled floor. On the disc in the lower and
outer quadrant a dark reddish brown patch, reaching to the disc
margin. It appeared to be situated deeply in the papilla. On
moving the head, parallactic displacement of the disc margin and
the patch was seen, so that the size of the patch appeared to vary.
An exactly similar case is recorded by Peltesohn.1

The disc depicted in Plate XLVII., Fig. 104, is apparently
an example of a condition analogous to those just described. The
whole disc area is larger than normal. The greater part of it is
deeply cupped, and the floor of the cup presents a pale crescent on
its outer side. It is to be noticed that there is an area of partial
atrophy of the choroid adjacent to the disc, as in Mr. Gunn's
case, and that, although the vision and the visual field were
normal, the other eye was blind from old (probably congenital)
choroiditis. The association suggests the possibility that the
deformity may be in some way connected with an inflammatory
process, occurring either before the disc is fully formed, or while
it is incapable of resisting an intraocular pressure slightly above
the normal.

A very similar condition of the disc, occurring in both eyes,
and associated with normal vision, has been depicted by Dolganoff.2

If the reader will now compare the illustrations representing
an abnormally developed connective tissue ring (Plate V., Figs. 12
and 14, and Plate VIII., Fig. 24) with those showing congenital
crescent (Plate VII., Figs. 18 and 19, and Plate VIII., Fig. 22),
and those of partial coloboma of the disc (Plate VIII., Fig. 25,
and Plate XLVII., Fig. 104), he will see that there are some
points of resemblance between these conditions. For example,
in all there is an abnormal relation between the connective tissue
and the nervous structure of which the disc is composed ; in all,
a part of the disc presents a peculiar dull-red colour ; and in all,
the vessels tend to emerge in an irregular manner.

1 Centralbl. f. prakt. Auyenli., Leipzig, 1888, p. 339.

2 Arch. f. Aucjenli., Wiesb., bd. xxviii.

PART II.

PATHOLOGICAL CONDITIONS.

' >

CHAPTER VI.

AFFECTIONS OF THE CHOROID.

In the first part of this work we reviewed the different conditions
of the fundus, which, as they are stationary and cause no
impairment of function, may be called “ Physiological Variations.”
We now pass on to deal with conditions which are Pathological.
The line of demarcation, however, is not well defined ; indeed,
a definition which should separate, with scientific accuracy,
pathological from physiological conditions, is impossible. For
practical purposes, we may consider as pathological such as are
progressive, or have been so at any time since birth, and such
as impair vision. This definition, however, if rigidly applied,
would include some cases of congenital malformation and exclude
others, and it would exclude some cases of intra-uterine disease
which have become quiescent before birth.

The sclerotic is not, as far as is known, the starting-point
of any morbid process in the fundus. Pathological conditions,
apart from affections of the head of the optic neive, are
therefore classed as choroidal or retinal, in accordance with what
is believed to be the primary seat of the disease.

The choroid and retina differ so greatly in structure that
there is seldom any difficulty in localising early changes in
the one or the other. But many affections begin in the one
coat and invade the other, and in an advanced stage of disease,
it is sometimes impossible, from the ophthalmoscopic appearances
alone, to determine which was first affected, although this can
usually be inferred from the experience afforded by other cases
in which the progress of the disease has been watched. Such
diseases are spoken of as choroido-retinal, or as retino-choroidal,

AFFECTIONS OF THE CHOROID.

the first word indicating in each case the tunic primarily
affected.

We have to deal, therefore, with the ophthalmoscopic
appearances produced by affections of the choroid, the retina,
and the optic nerve.

The choroid is, as we have seen, extremely vascular. A com-
parison between the number of vessels in its tissue, and the number
of the ciliary arteries which supply it, would also seem to show that
its circulation must be sluggish. Both these reasons probably
explain its great liability to degenerative processes and to chronic
inflammation ; while the large share taken by the choroid in the
ophthalmoscopic picture of the fundus renders the results of these
processes conspicuous. These results are usually classed as
choroiditis.

Choroiditis.

Choroiditis is, therefore, a rather wide term, since it is used so as
to embrace inflammation in actual progress, and the results of in-
flammation which has long since subsided. It includes affections that
may depend upon different causes, produce different changes in the
fundus, and affect vision to any degree between an impairment
that can be discovered only by careful examination and total
blindness. Attempts at classification have been made on the basis
of the supposed cause of the disease, on that of the ophthalmoscopic
appearances produced, and some varieties have even been named
after their discoverer.

No classification is entirely satisfactory, but we may conveniently
adopt two primary divisions — the suppurative, and the exudative
or plastic. The former might be called acute, the latter subacute
or chronic. Serous choroiditis was formerly believed to exist as the
cause of glaucoma and of detachment of the retina. There is,
however, no evidence that this view is correct, and the choroid
is not the kind of tissue that could be attacked by a serous

CHOROIDITIS.

inflammation in the sense in which that term is ordinarily
employed.

Atrophic choroiditis is a term sometimes applied to cases
characterised by the destruction of large areas of the choroid,
without much evidence of preceding inflammation. As, however,
most forms of choroiditis lead in their later stages to atrophy, it
will be more convenient to consider the condition as a result of
choroiditis, rather than as a separate variety.

Suppurative choroiditis occurs not infrequently as a result of
puerperal septicaemia. It is generally, if not always, due to the
presence of septic emboli in the choroidal veins. It rapidly leads to
inflammatory exudation into the vitreous, while at the same time
the conjunctiva often becomes acutely inflamed. The exudation
may break down into pus which may perforate the sclerotic, or the
vitreous may become converted into a solid, opaque mass, which
undergoes a certain amount of shrinking. In either case the eye
is rapidly lost.

It is conceivable that there may be an early stage in which
ophthalmoscopic examination would be possible. If so, the
opportunity does not appear to have been seized ; an omission
which is no doubt owing to the rapidity with which the media
become opaque, and also to the fact that the gravity of the
patient’s general condition masks the importance of the ocular
symptoms.

Exudative or plastic choroiditis is the most common form, and is
usually meant when the term choroiditis is used without any
qualification. The disease, as a rule, commences in different foci,
when it is called disseminated, but it may attack a large
extent of fundus at the same time, and is then called diffuse.
The distinction is to some extent artificial, for the disseminated
variety is often accompanied by diffuse changes, and a case
originally disseminated may at a later stage resemble the
diffuse variety, owing to the separate areas having increased in
size and become confluent. Still, the terms are useful, as they are
12

AFFECTIONS OF THE CHOROID.

descriptive of the ophthalmoscopic appearances at an early stage.
Moreover, the majority of cases of disseminated choroiditis remain
so throughout.

The term circumscribed choroiditis is sometimes used when the
disease is limited to an isolated portion of the fundus, other than
the macular region, while affection of this latter area is termed
central choroiditis. Other names, also, have been used to designate
minor variations, but they need not be enumerated.

Hypermmia of the choroid is sometimes described as an early
stage of choroiditis. Examination of eyes after removal shows that

Fig. 36. — Hyperaemia of the choroid from a recent wound of the eye.
(From a preparation by Mr. Treacher Collins.)

such a condition is exceedingly common, and occurs in a variety of
circumstances. Thus Fig. 36 is an example in which it was caused
by a recent injury ; while the case from which Plate XXXIII.,
Fig. 75, was taken, was one of leucocythsemia, in which distension
affected other vessels also.

The number of vessels in the choroid is so great that it seems
probable that even in health there may be considerable variations

DISSEMINATED CHOROIDITIS.

in the amount of blood that it contains. Such variations might
be brought about through vasomotor influences, and might also be
due in part to the presence of muscular tissue in the stroma of the
choroid.

But, although the amount of blood in the choroid is known to
vary in disease, and probably does so in health, there are no
ophthalmoscopic signs by which we can directly recognise these
variations. Even in such a disease as pernicious anaemia there
is no appreciable pallor of the fundus. In leucocythaemia the
colour of the fundus sometimes, it is true, appears orange rather
than red, but this is due to the change in the colour of the blood
and not to alterations in its quantity. In the case from which
Plate XXXIII., Fig. 74, was taken, there was no direct ophthal-
moscopic evidence of hyperaemia of the choroid.

Although hyperaemia of the choroid produces no appreciable
change in the colour of the fundus, it is probably sometimes the
cause of hyperaemia of the disc, for the colour of this is partly due
to vessels derived from the short ciliary arteries which also supply
the choroid. This no doubt explains why in some cases of
sympathetic ophthalmitis hyperaemia of the disc in the sympathising
eye is a prominent symptom. There is always, at the same time,
slight obscuration of the disc margin ; indeed, in the absence of
this it would be difficult to diagnose the hyperaemia with certainty.
An example of this was published some years ago by the
writer.1

Disseminated choroiditis , if it runs its complete course, passes
through the following stages, viz. : — (1) that of exudation ; (2)
that of atrophy ; (3) that marked by the existence of certain
complications.

The stage of exudation commences with the appearance of
small rounded areas of cell infiltration in the superficial layers
of the choroid. These, when rendered visible by thinning or
destruction of the retinal pigment over them, appear with the

1 Trans. Oplith. Soc., vol. iii., p. 73.

AFFECTIONS OF THE CHOROID.

ophthalmoscope as circular pale areas, which look as if the fundus
colour had been washed out (Plate XV., Fig. 40, Plate XX., Fig.
46, Plate XXII., Fig. 49).

These areas increase in size, maintaining a round or oval shape,
and usually become encircled by a more or less perfect line of
pigment. The increase takes place not only in superficial extent
but also in depth, so that the exudation may invade and replace
all the layers of the choroid.

The disease now passes into the atrophic stage. The exudation
undergoes degenerative changes and is absorbed. But the
structure of the choroid has been destroyed, so that on the
disappearance of the exudation, the sclerotic is exposed to view.
The pigment changes are, however, permanent, so that we now
see with the ophthalmoscope circular or oval areas of exposed
sclerotic, bordered by pigment which lies on a more superficial
level (Plate XV., Fig. 41, Plate XXV., Fig. 58). The appearance
will of course vary with the size of the atrophic areas. These
may still be small and separate, or they may have increased in
size to such an extent as to have come into contact, or coalesced
with each other (Plate XVI., Fig. 42).

If the morbid process continues it passes into what may be
called the stage of complications, although some of these
complications may supervene earlier. The retina now under-
goes extensive degeneration, and may become diffusely pigmented
(Plate XVII., Fig. 43, Plate XLV., Fig. 98). In this stage
connective tissue may form in the retina over the affected areas
(Plate XXV., Fig. 59). Meanwhile, the disease, spreading
forwards, reaches the ciliary region, and interferes with the
nutrition of lens and vitreous, causing opacities to appear in
both, while the iris often become adherent to the lens.

Eventually, the secretory function may be so impaired that
the intraocular tension becomes subnormal. At this stage the
lens usually becomes opaque, and all perception of light is lost.

The three stages of choroiditis, which have just been sketched,

STAGE OF EXUDATION.

may overlap, and therefore a single fundus often furnishes examples
of each. The progress of the disease is generally slow, and a
case may take many years to run its course. The majority of
cases come to a standstill before total blindness has been caused,
and such an arrest of the process may occur at any stage.

The ophthalmoscopic appearances caused by destruction of
choroidal tissue and by deposition of pigment are permanent.
Mere exudation, on the other hand, is likely to undergo some
absorption. If, therefore, the disease aborts in the exudative
stage, the changes in the pigment layer may alone persist (Plate
XVIII., Fig. 44, and Plate XIX., Fig. 45). If, on the contrary,
it is not arrested till the atrophic stage is reached, there will be,
in addition to the pigment changes, areas of exposed sclerotic
(Plate XXI., Fig. 48, &c.).

It must be remembered the arrest of the disease may be only
temporary, and that the later stages may be entered upon after
years of quiescence.

It is evident from what has been said that the ophthalmoscopic
appearances of choroiditis may differ widely. It will therefore
be necessary to consider in greater detail some of the more
common variations that are met with in each stage.

Stage of Exudation.

In this stage the spots of exudation may be of small size, and
distributed over the whole fundus, as in Plate XX., Fig. 46, or
they may be more numerous near the equator, as seen in
Plate XVIII., Fig. 44, which, however, represents a later stage
of the disease. It is often stated that disseminated choroiditis
usually commences at the periphery, but exceptions are certainly
very numerous.

The ophthalmoscopic appearance will, of course, also depend on
the size of the individual areas of exudation. In some cases they
remain exceedingly minute, even not exceeding the diameter of

AFFECTIONS OF THE CHOROID.

the primary retinal vessels. Such a condition is exceptional, and
might appropriately be called guttate choroiditis, had not the
term been applied to another condition.

The appearance will also depend upon the degree to which the
retina is implicated. In recent or relapsing cases the retina is
sometimes oedematous over the affected area (Plate XXV., Fig. 58).
This condition wall be considered in dealing with the stage of
complications. Changes in the retinal pigment are so commonly
present at all stages that they will be more conveniently dealt
with here.

Probably in all except the lightest eyes, some destruction of
the pigment layer is necessary before the exudation becomes
visible. This de-pigmentation may be limited to the affected
spots, or may occur over a considerable area of the fundus, causing
the choroidal vessels to become visible. The latter is seen in
Plate XX., Fig. 47 ; and Plate XLV., Fig. 98, which represent a
later stage.

More conspicuous ophthalmoscopic changes are caused by the
deposition of pigment over and around the exudation. It is only
exceptionally in ordinary disseminated choroiditis, that this
pigmentation does not occur as in Plate XX., Fig. 46 ; Plate XXI.,
Fig. 48 ; Plate XXII., Fig. 49. In the form of choroiditis that
complicates progressive myopia, on the other hand, large areas
of choroid undergo atrophy with little or no pigment deposit
(Plate XXIII., Figs. 53, 54, 55), hence the occasional application
of the term atrophic choroiditis to this condition.

The pigment deposit in some cases is excessive, and when the
disease subsides, it may form the most prominent appearance, as
in Plate XVIII., Fig. 44; Plate XIX., Fig. 45.

The pigment usually forms rings or discs of nearly circular
shape. Exceptionally, it may be irregularly deposited, as in
Plate XLII., Fig. 95. This, however, was drawn from the eye
of an Eurasian, and it is probable that the dark races would
present pigment changes different from those commonly met with

ATROPHIC STAGE .

in Europeans. The material at my disposal, however, is too
limited to justify any positive conclusions on this point.

Atrophic Stage.

The appearance presented in the stage of atrophy will largely
depend upon the course run by that of exudation. If arrest
of the disease has occurred wdiile the spots were still small,
numerous small white areas of nearly circular shape will be seen
scattered over the fundus, each surrounded by a ring of pigment.
This form of the disease seems to occur most frequently in
inherited syphilis, and the ophthalmoscopic appearances are often
first discovered when the cornea begins to clear after an attack of
interstitial keratitis, — a fact that should induce caution in giving
a prognosis as to recovery of vision, even when the corneal
affection is comparatively slight. In this variety the choroidal
plaques seen are usually most numerous towards the periphery,
although the central region enjoys no immunity.

Sometimes pigment deposit around the patches is delayed,
or does not occur ( Plate XXI., Fig. 48). It is, however, quite
exceptional for the atrophic stage to be reached without some
deposition of pigment taking place.

If the disease be not arrested early, the areas of exudation
increase in size, come into contact with, and then merge into, each
other, while pigment, if absent before, is generally now to be seen
bounding the patches of atrophy. The transition from the exudative
to the atrophic stage will be evident by comparing Plate XX., Figs.
46 and 47, which represent the same case at the two stages. The
interval between the time of making the two drawings was two
and a half years. When the patches have attained a considerable
size, and have undergone complete atrophy, they may continue
to increase without evidence of fresh exudation, probably because
the destruction of a large number of the choroidal capillaries
interferes with the nutrition of the adjacent tissue, so that it

AFFECTIONS OF THE CHOROID.

readily becomes atrophied. In this way immense tracts of the
sclerotic may become denuded, as in Plate XVI., Fig. 42, and
Plate XVII., Fig. 43.

The atrophic stage is, however, best seen in high and pro-
gressive myopia. In the majority of cases in which the myopia,
although high, is stationary, there is at the outer side of the disc
a crescentic area of choroidal atrophy, which allows the sclerotic
to be visible (Plate XXIII., Fig. 53). The existence of this
myopic crescent, as it is called, usually indicates that protrusion
of the coats of the eyeball at its posterior part, which is called
posterior staphyloma. Hence the crescent itself often goes by
this name. The crescent may have a cleanly-cut, regular outline
(Plate XXIII., Fig. 53), in which case the myopia is probably
stationary. On the other hand, it may have an ill-defined and
irregular boundary passing imperceptibly into the choroid (Plate
XXIII., Fig. 54). In this event the myopia is progressing, and
it is probable that in time separate areas of choroidal atrophy
will appear beyond the limits of the crescent. As the latter
increases the atrophic areas may coalesce and a large irregular
patch of sclerotic lie exposed to view.

While the convexity of the myopic crescent is thus extending
in the direction of the macula, its arms spread gradually further
round the disc, till meeting they may encircle it by an atrophic
ring, which may subsequently increase in breadth.

The atrophic patches which result from disseminated choroiditis
are often incomplete, since some large choroidal vessels are
generally to be seen crossing them. In the atrophy associated
with progressive myopia the destruction of the choroid is,
on the contrary, usually complete. Pigment deposit, also,
which is the rule in disseminated choroiditis, is the exception
in myopia.

These cases of progressive myopia are obviously of a difierent
nature from the simple non-progressive form. The latter may be
looked upon as an exaggeration or perversion of the physiological

STAGE OF COMPLICATIONS.

increase of refraction which occurs in early life. Progressive
myopia, on the other hand, is essentially a morbid process.

A peculiar displacement of the vessels on the disc is said to
be common in myopia. The condition referred to is not present
in either of the myopic eyes shown in Plate XXIII., but it will
be seen in Plate XI., Fig. 30, which represents a hypermetropic
eye. In the opinion of the writer, this arrangement is not so
frequently associated with myopia as generally stated, and is
certainly often met with under other conditions.

Atrophy of a zone of choroid immediately around the disc
sometimes occurs as a degenerative change in old people ; an
example of this is seen in Plate XXIV., Fig. 56. A much
narrower zone of atrophy is commonly met with in advanced
cases of chronic glaucoma (Plate XLVII., Figs. 105, 106, and
107).

Atrophy of the pigment layer of the retina round the disc is
not an uncommon sequence of post-neuritic atrophy, and occasion-
ally the disturbance extends into the substance of the choroid, as
in Plate XXIV., Fig. 57, and Plate XXXII., Fig. 71.

Stage of Complications.

Implication of the pigment layer of the retina is so common
in choroiditis that it can hardly be considered a complication
so long as it is limited to the affected areas.

Diffuse pigment changes, however, sometimes occur, consisting
both in deposition and removal of pigment. An example of the
former is seen in Plate XVII., Fig. 43, and of the latter in Plate
XX., Fig. 47, and Plate XXIV., Fig. 56.

The bacillary layer of the retina is affected early in most
cases of choroiditis. Owing to the transparency of the retina, this
cannot be diagnosed with the ophthalmoscope, but it may be
inferred to have taken place from the impairment of vision.

In a late stage of the disease extensive degenerative changes
13

AFFECTIONS OF THE CHOROID.

may occur in the retina, leading to destruction of its nervous
elements, and increase in its connective tissue. The retinal
vessels will now be much shrunken, and the disc assume a dull
dirty-white colour like parchment. At this stage pigment may
find its way forwards through the layers of the retina, and on
reaching the surface, assume the stellate arrangement that exists
in retinitis pigmentosa. The ophthalmoscopic picture may now
exactly resemble that of retinitis pigmentosa, while the subjective
symptoms of night blindness, and contraction of the visual field,
which characterise that disease, may also be present. (Compare
Plate XIX., Fig. 45, Plate XLII., Fig 94., and Plate XLIII.,
Fig. 96.)

(Edema and inflammatory exudation are met with in the
retina in some cases of acute choroido-retinitis occurring in the
secondary stage of syphilis. When oedema occurs in a chronic
case, it indicates the formation of a fresh patch of choroiditis.
The soft-looking white colour, shading off into the adjacent
fundus, is characteristic, and is seen in Plate XXV., Fig 58.

The retinal vessels may pass unchanged over an cedematous
area, or their calibre may appear to be irregularly diminished,
owing to the vessel being partly concealed from view in places
where it happens to be less superficial than usual.

A variety of choroiditis, in which retinal oedema is a prominent
feature, occurs in association with isolated patches of old choroidal
atrophy. The subjects of this affection are usually young adults
of sedentary habits and ansemic aspect. The condition has no
connection whatever with syphilis, but a family history of tubercle
can often be elicited. In the course of a few weeks the oedema
clears up, and there is exposed to view a patch of partial or
complete atrophy of the choroid.

The occurrence of retinal oedema may also mark the com-
mencement of a more diffuse choroiditis, as will be seen from
the history of the case from which Plate XXIX., Fig. 63, is
taken.

STAGE OF COMPLICATIONS.

In a late stage of choroiditis, masses of connective tissue form
in the retina. These probably indicate adhesion between the two
membranes, and may be looked upon as cicatricial in character.
The macular region is most commonly affected. The cicatricial
material may consist of a large irregular patch, with processes
jutting out from it, and running into the retina in different
directions. Or it may present numerous round or oval
openings as in Plate XXV., Fig. 59. In either case the border
of the patch presents bays, with regular curves, the con-
cavities of which are directed away from the centre of the patch.
The colour of these cicatricial masses resembles that of exposed
sclerotic, but is a more dead white, and lacks the bluish tinge of
sclerotic. The presence within the white area of round or oval
patches of comparatively normal fundus, evidently lying on a
deeper level, is characteristic.

This condition must not be confounded with that which has
been described by Manz as Retinitis Proliferans ; in this latter
the exudation lies in front of the retinal vessels.

The complications of choroiditis are by no means limited to
the retina. Opacities in the vitreous may be present at any
stage of the disease. When they occur early, as is frequently
the case in choroiditis of syphilitic origin, they are usually
situated in the forepart of the vitreous, and are fine — “ dust-like.”
They are either fixed, or but slightly moveable. Such opacities
blur the fundus, but are easily overlooked owing to their small
size and forward position. To see them well, a convex lens is
required behind the ophthalmoscope, and they are often more
conspicuous with a plane than with a concave mirror. The
blurring of the disc produced by such opacities is often mistaken
for optic neuritis, but it should be noted that there is no dis-
tension or tortuosity of the retinal vessels, and no evidence of
swelling of the disc.

In the later stages of choroiditis, the opacities met with are
larger, and form dark threads or masses of irregular shape. They

100

AFFECTIONS OF THE CHOROID.

can be made to float about freely in the vitreous, by directing
the patient to move his eye rapidly, and then to look fixedly in
one direction. Such opacities may lie at any depth. Their dark
colour is, of course, due only to the interception of the light
reflected from the fundus ; if the}^ are of large size, and placed
far forwards, light is often reflected from their surface, and they
then appear to be white or grey. The wide excursions made by
these opacities indicate that the vitreous has become abnormally
fluid.

At this stage opacity of the lens is not uncommon. It
usually commences as a posterior polar cataract, i.e., a central
opacity of the posterior pole which may have strise radiating
from it. This may remain unchanged for an indefinite time, or
the whole lens may become opaque, and assume the dead-white
chalky appearance which is met with only in blind eyes.

By this time posterior synechim will have formed. At first
these are fine and thread-like, but later there may be total
adhesion between the iris and lens. Throughout the progress
of the case the ciliary injection, which we are accustomed to see
in ordinary plastic iritis, is usually absent.

At any stage fine dots, keratitis punctata, may appear
on the posterior surface of the cornea. These may clear off and
reappear many times. Their presence interferes mechanically
with vision, but they do not appear to be accompanied by any
perceptible increase of the fundus mischief. They always indicate
that the disease has reached the anterior part of the uveal
tract.

In the latest stage the function of the secretory apparatus
becomes impaired or destroyed, and the intraocular tension sub-
normal. Detachment of the retina is then likely to occur. The
reason that this complication is not present more frequently in
choroiditis is probably the formation of adhesions between the
choroid and retina.

In a few cases the vitreous contracts and draws the lens and

CHOROIDITIS OF THE MACULAR REGION.

101

iris backwards ; the anterior chamber then has an enormous
depth, while the iris, being seen through a great depth of aqueous,
(which, with the cornea, acts like a convex lens), has a peculiar
brilliant appearance.

Choroiditis of the Macular Region.

The reader will have gathered from the illustrations already
referred to that in disseminated choroiditis the yellow spot region
often remains unaffected. This is due to the fact that the disease
usually commences in the equatorial region, and spreads slowly.
The macular region may, however, be involved either by extension
from the periphery, or primarily.

Forster1 has given the name areolar to a form of choroiditis
which occurs in this region, and presents the appearance of
numerous round or oval areas of choroidal atrophy with inter-
vening normal fundus. It usually affects a considerable area,
and appears to differ in no essential respect from disseminated
choroiditis.

There are other forms of central choroiditis which are more
definitely confined to the macular region. Old persons are
especially liable to choroiditis of this part of the fundus, a fact
that should always be borne in mind in forming a prognosis as
to the result of extraction in cases of senile cataract.

Central senile choroiditis appears in two forms. In the one
there is de-pigmentation of a circular area of the fundus, having
a diameter of about twice that of the optic disc. Over this area
the superficial layers of the choroid undergo atrophy, so that the
larger choroidal vessels become visible. I have not been able to
secure a typical illustration of this condition ; but a good example
will be found in Wecker and Jaeger’s atlas, Fig. 97, while a more
advanced stage has been shown by Mr. Nettleship.2 The other
form resembles disseminated choroiditis, but the affected areas

1 Ophth. Beitr., Berlin, 1862, p. 97.

2 Trans. Ophth. Soc., vol. iv., p. 165.

102

AFFECTIONS OF THE CHOROID .

are smaller and more closely aggregated. Plate XXII., Fig. 50,
is an instance of this.

The progress of the disease being slow, and the patients old,
an opportunity of tracing the malady through its various stages
seldom arises. A large area of atrophied choroid is, however,
often met with, which must be the result of choroiditis in
the central region. In such cases the sclerotic often has the
appearance of being pushed backwards. The whole patch is
usually encircled by pigment, which also sometimes forms an
irregular trellis-work over the patch and at a little distance in
front of it.

Almost complete absence of the choroid at the macula is
occasionally met with in young people. In some of these the
defect is probably congenital. Examples of this are seen in Plate
XXII., Figs. 51 and 52. Both were from young and healthy
women, who had only recently discovered that the vision of one
eye was defective ; but from the advanced condition of the changes,
it is obvious that they were not of recent date. Although the
affected areas differ in size, they present many points of similarity.
In both, there is an area of sclerotic completely exposed, crossed
by choroidal vessels. In both, this is bounded by a pigment ring,
which overhangs it, and with the ophthalmoscope was obviously
anterior to it. The pigment forms a network with numerous
openings, through which the sclerotic is visible. In Fig. 53 the
area of pigment deposit is considerably larger than that of the
atrophy.

Such cases as these are considered by many to be examples
of defective development of the choroid, and hence are called
coloboma of the yellow spot. It seems to me that the
presence of extensive pigmentary changes renders this view
highly improbable, and that the presence of choroidal vessels
disproves it. It is more probable that the condition is the
result of a localised choroiditis occurring in early childhood.

Isolated patches of choroiditis, or the results of former attacks,

—

CHOROIDITIS OF THE MACULAR REGION.

103

may be met with in any part of the fundus. It is possible that
some of these isolated areas are the result of haemorrhage.

There is, however, ground for suspecting that these large
isolated areas of choroidal atrophy at the macula or elsewhere,
represent the site of former tubercular deposits.

Stephen Mackenzie1 has published the case of a girl, four years of age, who had
been ailing for eighteen months before coming under observation, with frequent feverish
attacks, headache and vomiting, and chronic disease of knee. Shortly before admission
sight became defective.

She was found to have double optic neuritis. In the macular region of LE. was a
patch, larger than the disc, of yellowish colour, bordered by pigment, and a slightly smaller
patch in a more peripheral situation ; in RE. were several smaller patches. None of them
appeared to be much raised.

The child had a continuously high temperature. Later, she became drowsy, had
convulsions, and died after being in the hospital about five weeks.

At the post-mortem, which was confined to the head, a quantity of yellow lymph was
found at the base of the brain. Some miliary tubercles at the base of the brain, and in
the fissure of Sylvius. There were several masses of tubercle in the brain substance.
Microscopic examination of these showed the characteristic appearance of aggregated
tubercle. The pia mater was everywhere occupied by tubercular infiltration. The trunk
of the optic nerve was infiltrated throughout the whole length examined with round cells.
The patches in the choroid showed a number of small round cells, and in places, tubercles
containing giant cells. Tubercle bacilli were not found either in the choroidal or in the
cerebral nodules, but there can be no reasonable doubt as to the tubercular character of
the latter, and the microscopical characters of the choroidal areas were obviously identical
with them.

Occasionally, large tubercular masses have been found growing
from the choroid. For example, in the discussion on the above,
Dr. Barlow 2 mentioned a case in which an eye was excised for
an intraocular growth, which, on examination, proved to be a
hemispherical mass of tubercle, reaching from the disc to the
ora serrata, and presenting the character of confluent tubercle.
The child died a year later with cerebral symptoms, and caseous
tubercular growths were then found in the brain and bronchial
glands. Mr. Brailey also stated, in the same discussion, that he
had found a growth, the size of a pea, having the structure of
tubercle, near the optic disc in an excised eye. The patient

1 Trans. Ophth. Soc., vol. iii., p. 119.

2 Loc. cit.

104

AFFECTIONS OF THE CHOROID.

presented no other symptoms of tubercular affection, and the
subsequent history is unknown.

Carpenter, in a paper on this subject,1 2 has given illustra-
tions of the ophthalmoscopic appearances of several cases in
which the history pointed to the choroiditis being of tubercular
origin.

How far contusions of the eye are capable, apart from
haemorrhage, of starting progressive changes in the choroid, is
at present doubtful. It is seldom that conclusive evidence can
be obtained that the fundus was normal before the accident, and
it must also be remembered that pigmentary disturbances of a
degenerative character may occur in any blind eye. For these
reasons, cases of choroiditis attributed to injury must be accepted
with caution. This subject will be referred to again in dealing
with rupture of the choroid.

An affection of the choroid, more superficial than those yet
described, produces an ophthalmoscopic appearance of rather
closely aggregated pale-yellowish dots, with soft outline. These
are most numerous in the macular region, to which they may
be entirely confined.

Attention was first directed to this condition by Hutchinson
and Waren Tay/ It is commonly called “ Tay's Choroiditis/'
The cases first described occurred in persons who were
past middle life, and the condition was thought to be of a
degenerative character. Similar ophthalmoscopic appearances
have, however, been met with in patients of all ages. The
affection commences in the superficial layers of the choroid,
probably in the lamina vitrea ; it tends to spread forwards into
the pigment layer of the retina, and not backwards into the true
structure of the choroid. For this reason, and also because the
ophthalmoscopic appearance is similar to that produced by other

1 “Tuberculosis of the Choroid,” 1890.

2 Ophth. Hosp. Rep., London, vol. viii., p. 231, 1875.

DIFFUSE CHOROIDITIS.

105

conditions, which are believed to be situated in the retina, further
consideration of these cases will be deferred till we come to deal
with retinal affections.

Diffuse Choroiditis and Choroido-Retinitis.

The early stage of diffuse choroiditis is characterised by large,
pale coloured, areas on the fundus (Plate XXIX., Fig. 63). These
are of various sizes, of irregular shape, and are separated by
spaces of healthy-looking fundus. The patches are largest and
most numerous towards the periphery. Some form complete
islands, while others of larger size, have an irregular outline,
indented with bays, and fissured by tracts of healthy fundus. A
fancied resemblance of the whole distribution to a continent
bounded by an irregular coast line, beyond which are numerous
islands, has led to this form of choroiditis being sometimes
described as “ map-like.” Many of the areas resemble oak leaves
in shape, and the term “ leaf-like ” has also been employed.

The changes have a superficial appearance. There is no
border of pigment to the patches, although some mottled pigment
can sometimes be seen on their surface, while over others, which
are of older date, the pigment layer is completely destroyed.

The progress of these cases is so slow that it is difficult to say
what is their ultimate fate. Plate XXIX., Fig. 63, was taken
from a young man, of rather delicate appearance, but presenting
no physical signs of disease. There was no history of syphilis,
congenital or acquired. During the two years he was under
observation no appreciable changes occurred in the ophthalmo-
scopic appearance. In this case the choroiditis was preceded by
retinal oedema.

Later in life we meet with diffuse choroidal changes, of which
some probably represent a later stage of the condition just
described, while others may be the outcome of disseminated
choroiditis. The course of the disease is exceedingly chronic
14

106

AFFECTIONS OF THE CHOROID.

The patients affected, if not old in years, are of senile aspect, and
the majority are the subjects of tertiary syphilis. The disease
should therefore be looked upon as being of a degenerative,
rather than an inflammatory character, and might be described
as a choroido-retinal sclerosis.

The appearance presented, although of course varying to some
extent in different cases, is sufficiently uniform and characteristic
to render the diagnosis easy. In some points it resembles
retinitis pigmentosa ; the condition has therefore sometimes
been called choroido-retinitis pigmentosa. If the reader will
compare Plate XXVI., Fig. 60, with Figs. 61 and 62, he will
readily see that all have certain features in common. Over
the greater part of the fundus the choroidal vessels are visible.
Nowhere is the structure of the choroid destroyed in its whole
thickness, so that these vessels are exceedingly numerous. In
many places, and especially near the disc, their walls have
undergone a change which has rendered them opaque, so that they
appear white. As in the case of similar changes in the retinal
vessels, there is no reason to suppose that they are obliterated.
A few of these vessels are accompanied by white lines (Plate
XXVII., Fig. 61) ; in some cases these are much more numerous
than in the illustrations. It will be noted the red fundus colour
is replaced by a reddish brown. This is no doubt due to exposure
of the stroma of the choroid by the destruction of the capillary
layer : in a few places where the latter remains, it is seen covering
the surface like a red veil.

There is a certain amount of pigmentation of the retina
resembling that which is present in retinitis pigmentosa, but it is
more massive and not specially abundant at the periphery as in
that disease. In Plate XXVIII., Fig. 62, the pigment appears
to a great extent to be deposited in the choroid itself, and the
retinal vessels are more diminished than in the other cases. The
circular white areas appear to consist of congeries of vessels, but
it is not clear why they assume this form. In Plate XXVI.,

CH OR 01 D O-RE TINA L SCLEROSIS.

107

Fig. 60, there is some circnm-pap i llary atrophy, and the disc is of
a dirty hue, while in Plate XXVII., Fig. 61, which represents a
less advanced condition, these features are absent.

The subjective symptoms vary much, and correspond but
little with the ophthalmoscopic appearances. It is, indeed, not
uncommon to find similar appearances in the two eyes of the
same patient associated with great differences in vision. Usually,
the impairment of vision is not as great as might be expected
from the ophthalmoscopic changes. This is in part to be explained
by the fact that the macular region is less changed than the rest
of the fundus. There is generally night blindness, and the fields
are often contracted. In the case from which Plate XXVII.,
Fig. 61, was taken these symptoms were absent, and the vision
was normal. Stanford Morton has described and depicted a
marked case1 in which, while central vision was normal, night
blindness and contraction of the visual fields were present.

The ophthalmoscopic appearances are due to a diffuse affection
of the choroid, attacking primarily its more superficial vascular
layers, and invading the retina secondarily. The alterations in
the walls of the choroidal vessels, and the limitation of the
changes in the early stages to the neighbourhood of the disc,
point to a degenerative disease of the short ciliary arteries as
the immediate cause of the fundus changes. As to the more
remote causes we know little. Among them must no doubt be
reckoned tertiary syphilis and senility, but it is not improbable
that any widespread affection of the choroid, such, for example,
as that depicted in Plate XXIX., Fig. 63, might be followed in
after years by the condition under consideration.

In one patient who was under the writer’s care the condition
followed retinal haemorrhages. The case is so unusual that the
details may be of interest.

John H., 67. First seen July 1890 with a history of a sudden failure of vision having
occurred three weeks previously in the RE. There were numerous haemorrhages scattered

1 Trans. Ophth. Soc., vol. v., p. 142.

108

AFFECTIONS OF THE CHOROID.

over the retina, chiefly in the fibre layer. The condition resembled that shown in Plate
XXXV., Fig. 79, which was taken from another patient. The condition of the vision was
not noted.

Fourteen months later OR. atrophic ; white lines along the retinal vessels. White soft
areas on retina, probably altered hremorrhages. V. = hand movements.

In January 1893 — 2| years after the attack — choroidal vessels visible over whole
fundus. OR. atrophied. Superior temporal vein accompanied by white bands. P>elow YS.
a patch of dirty grey colour, from which straight processes passed in several directions.
Below the superior temporal vein a circular white area like those seen in Plate XXVII.,
Fig. 61, but smaller. LE. remained normal throughout. The patient was seen in June,
1895, and was in the same condition as before.

The next case shows that a similar condition may result from
disseminated choroiditis.

Henry P. Had been, in 1881, under the care of Mr. Nettleship, who kindly furnished
me with particulars of his condition at that time.

No history of syphilis could he obtained. He married at the age of 18, and had six
children ; three are living and said to be in good health. (The deaths of the others had no
bearing on the case.) He has never been out of England ; he lived in Bedfordshire till
1854, since then in London.

With the exception of attacks of acute rheumatism in 1865, 1869, and 1874, he has
always had good health.

He was a letter carrier by occupation. He thinks that his sight has never been
“ strong,” but he first noticed a definite failure at the age of 22. It appears to have been
slight, and to have increased very slowly, if at all, until the age of 44, when it became
rapidly worse. He went to St. Thomas’ Hospital, where he was found to have dis-
seminated choroiditis chiefly in the central region. The fields were approximately
normal. He attended off and on for two years without any appreciable alteration taking
place. In 1890 he came under the writer’s notice at the Royal Westminster Ophthalmic
Hospital.

He was at this time 53 years old, anaunic in appearance, fair, with sandy hair turning-
grey. Vision LE. = N, and it has remained nearly constant. V. of RE. has fluctuated
without obvious cause. In 1890 it was N ; in January 1891, October 1891, the same;
January 1892, in 1894, 6 Sn. at 20 cm. Visual fields nearly normal in extent. No
night blindness. Knee jerks absent. No other indications of ataxy.

The ophthalmoscopic appearances in January 1896 had not appreciably altered since
he was seen in 1890, and were as follows : —

LE. OR. pale, retinal vessels normal, edge of OR. a little hazy. In central region, over
an area with ill-defined boundary measuring roughly 4 dd., numerous choroidal vessels
visible. The greater number are pale — nearly white ; some of these have a central red
streak. Towards the periphery of the affected area there are several red vessels of normal
size bounded by white lines. There are a few masses of pigment on- the surface of the
affected area. The spaces between the vessels are very small, and of light brown colour.
In periphery of fundus no choroidal vessels are visible, but there are several deposits of
pigment, mostly in the form of streaks.

The condition of the RE. is similar but less marked, and OR. is not pale.

CAUSES OF CHOROIDITIS.

109

Causes of Choroiditis.

Syphilis, both hereditary and acquired, is certainly the most
frequent cause of choroiditis.

The choroiditis which results from hereditary syphilis, is often
first discovered as an attack of interstitial keratitis is clearing
up, and in the majority of instances there is no reason to suppose
that it existed prior to the corneal affection. It is most probable,
in such cases, that it is the ciliary part of the uveal tract which
is primarily affected, and that the disease spreads thence both
to the cornea and to the choroid. The case may, however, be
uncomplicated throughout by any corneal affection. Cases of
choroiditis undoubtedly occur in young subjects in whom there
is no reason to suspect a syphilitic taint as in Plate XV., Fig.
40 ; in such the disease would seem as a rule to be limited in
extent, and to become quiescent early.

The choroiditis of acquired syphilis may occur at any time
after the period of the skin affection. It usually follows it within
a few months, but sometimes not till years afterwards.

A feature which is fairly constant in syphilitic choroiditis is the
circular shape of the patches, and the completeness with which the
affected areas of the choroid become atrophied, so that the fundus
is dotted over with punched-out round holes. This feature will,
of course, be absent if the patches have become confluent. It is
due to the mode in which the disease begins, viz., from circular
nodules of exudation, analogous to gummata.

Cases of syphilitic choroiditis occurring early in the course
of the disease are sometimes accompanied by cedematous or
inflammatory changes in the retina, and by the presence of very
fine dust-like .opacities in the anterior part of the vitreous.
The concurrence of these conditions may generally be taken to
indicate that the disease is of syphilitic origin. But choroiditis
occurs, and that not very rarely, in cases Avhere syphilis may be

110

AFFECTIONS OF THE CHOROID.

excluded, and I know of nothing in the character of choroiditis,
apart from the points just mentioned, which will serve to indicate
whether it be of a specific nature or not.

Tubercle, as a cause of choroiditis, appears to me not to have
received the amount of attention which it deserves. Tubercular
iritis is a recognised condition, particularly in young subjects, and
tubercular foci of inflammation are met with in the choroid in
many cases of tubercular meningitis, and disseminated tuber-
culosis ; such differ in no essential respect from spots of early
disseminated choroiditis. It is true that they are usually of
small size, and rather more raised, but such differences may be
explained by the fact that the disease is always recent, and
probably very active. The general disease being so fatal, the
opportunity of watching the progress of the choroidal affection
is not likely to occur often, and I do not know of any case in
which this has been done.

Bearing in mind the frequency of tubercular affections of
glands and joints, it might be well to consider whether many
hitherto unexplained cases of choroiditis have not had a similar
origin.

In dealing with large isolated patches of choroiditis, we gave
reasons for believing that some of them were the result of
tubercular masses which had undergone degeneration. It is quite
likely that smaller areas may be due to a similar cause, and
it is certain that tubercles in the choroid are not confined, as
they were at one time believed to be, to cases of miliary
tuberculosis.

Rheumatism has been suggested by Leber 1 as a cause of
choroiditis. Personally I am not acquainted with any evidence
which supports the view that choroiditis is more common in
rheumatic subjects than in others.

1 Helmholtz, “Festschrift,” Art. xii., 1892.

RUPTURE OF THE CHOROID.

Ill

Rupture of the Choroid.

Blows upon the eye sometimes cause a tear in the choroid ;
the rent usually lies in the neighbourhood of the disc, and runs
in a direction roughly concentric with its margin. At first
it may be impossible to diagnose the lesion, because blood is
poured out from the torn vessels, but when this is absorbed, the
rupture is seen as a narrow band of exposed sclerotic, over which
the retinal vessels pass unchanged. Pigment is often accumulated
at the margins of the rent. The condition is now to be distin-
guished from atrophy, the result of choroiditis, only by the shape
of the patch and the history of injury.

Irregular areas of choroidal atrophy may be met with in
patients who give a history of an injury, and such are frequently
diagnosed as ruptures of the choroid. It must not be forgotten
that an injury often draws attention to a defect already present ;
still, it seems not improbable that in some of these cases the
injury has caused choroidal haemorrhage, and that the effused
blood has led to atrophy of the choroidal tissue.

Although some ruptures of the choroid remain unchanged for
years, others show a tendency for the exposed sclerotic to become
pigmented. For example, in the case shown in Plate XXX.,
Fig. 64, seven months after the injury the borders of the patch
were pigmented, and a month later its whole surface was of a
steel grey colour.

In a case published by Benson,1 the rupture, when seen
three weeks after the injury, was cream-coloured, and there was
no trace of haemorrhage or pigmentation. A month later the
area of the rupture was darkly pigmented, and there were a few
spots of choroidal atrophy scattered about.

The shape of the rupture in Plate XXX., Fig. 65, is unusual,

1 Trans. Ophth. Soc., vol. ii., p. G2.

112

AFFECTIONS OF THE CHOROID.

and beyond it are three isolated pale areas, which may be
presumed to be tears in the choroid. The connection of the
condition with the injury admitted of no doubt, as when the
eye was first seen the vitreous contained blood. Unfortunately
the progress of the case could not be followed.

The shape of the rupture is probably in some way dependent
upon the firm connection between the choroid and the disc, but it
is not easy to see what determines its position.

In cases of old choroido-retinitis, white bands, probably
cicatricial, are sometimes seen on the fundus. These bear some
resemblance to rupture of the choroid (Plate XLV., Fig. 98),
but they are usually straight. Two cases recorded by Kenneth
Campbell as examples of equatorial rupture of the choroid should
be compared with these cases.1

The fact that the rupture becomes pigmented, and that
separate areas of choroidal atrophy are often found associated
with rupture, raises an interesting question as to the extent to
which a contusion of the eye is capable of causing fundus change
apart from typical rupture of the choroid.

Siegrist 2 has recently suggested that the areas of partial
choroidal atrophy near the disc, occasionally seen after con-
tusions of the eye, are secondary to rupture of the short
ciliary arteries. He gives illustrations of four cases which
presented the following features in common : — (1) An injury
from a blunt body ; (2) yellowish decoloration of an irregular
map-like area adjacent to the disc ; (3) an interval of a few
weeks between the receipt of the injury and the full
development of the atrophic area, which afterwards remains
unchanged.

In the case depicted in Plate XXX., Fig. 04, it will be
observed that there are several small patches about the disc,
where choroid is defective. It is doubtful whether these were

1 Tran*. Oplith. Soc., vol. xii., Plate ArII., and vol. xv., Plate IX.

2 Mittli. a. Klin. u. med. Inst. d. Schweiz, Basel u. Leipzig, bd. iii., p. 9, 1895.

RUPTURE OF THE CHOROID.

113

due to the injury or had existed previously. In the former case
the above explanation might account for them.

A case of pigmentation of the retina following concussion
of the eye, which was recorded by J. Hutchinson, jun.,1 was
probably also of this nature.

1 Trans. Ophtli. Soc., vol. ix., p. 116.

CHAPTER VII.

OPTIC NEURITIS OR PAPILLITIS.

The intraocular termination of the optic nerve — the so-called
optic disc — is the only part accessible to ophthalmoscopic
examination. Changes, therefore, may be present in the

optic nerve or tracts, in the nerve centres, or in any link
of the chain connecting these, without giving rise to any
ophthalmoscopic signs, even though they may be sufficiently
pronounced to cause complete blindness. At the same time,
lesions which are situated anterior to the chiasma usually initiate
degenerative changes, which, creeping down the nerve, eventually
become recognisable at the disc. Any injury of the optic nerve
that interferes with the local circulation is rapidly followed by
conspicuous changes in the disc and retina. On the other hand,
lesions posterior to the chiasma do not, as a rule, cause atrophic
changes in the discs. But owing to the semi-decussation of the
centripetal nerve fibres in the chiasma ( see Fig. 37, page 115), they
may cause defects in the visual fields of both eyes (hemianopsia).

It should not be forgotten that the chiasma, besides affording
an opportunity for the redistribution of the nerve fibres from the
two retinae, also acts as one of the commissures connecting the
two halves of the brain. The commissural fibres indeed form about
a third of the entire mass of the chiasma.

Many intracranial conditions cause inflammatory changes in
the disc, a fact that will excite no surprise when we bear
in mind the short course of the optic nerves, their direct
continuity with the brain substance, and the intimate con-
nection which subsists between their sheaths and the cerebral
meninges.

DEFINITION OF TERMS.

115

It must always be remembered that the visible changes in the
disc may be merely part of a lesion of the nerve trunk, and as we
cannot see beyond the lamina cribrosa and ascertain the state
of the optic nerve by direct inspection,
the prognosis is necessarily doubtful.

We have seen that choroiditis com-
monly leads to atrophy of the choroidal
tissue, and that the resulting ophthal-
moscopic appearances are conspicuous
and characteristic. In the retina, on
the contrary, atrophic changes neither
occur so readily, nor are they so con-
spicuous. This latter fact is due to
the transparency of the retina, which Fig 37._Diagram showing the
renders it practically invisible. Atrophy semi-decussation at the chiasma.

of its tissue can therefore only be re- , A TTf°fn of ,ng:ht traofc causing loss of

J left half of each visual field.

cognised with the ophthalmoscope when

it is accompanied by changes in the pigment layer, or by diminution
in the size of the retinal vessels. These changes occur in many
degenerative conditions, but usually only at an advanced stage.

Inflammatory conditions, on the other hand, rapidly produce
visible changes in the retina, which are largely due to loss of its
transparency, and to obstruction to its circulation.

Inflammation of the intraocular termination of the optic nerve
is commonly spoken of as optic neuritis. The term papillitis more
accurately indicates the localisation of the visible changes in the
optic disc or papilla, but is not yet in such general use.

When there are inflammatory changes both in disc and retina
the condition is called neuro-retinitis.

Inflammation of the trunk of the nerve behind the globe,
without implication of its intraocular termination, is indicated
by the term retro-bulbar neuritis.

In order that the significance of the ophthalmoscopic appear-
ances presented in these conditions may be appreciated, a

116

OPTIC NEURITIS OR PAPILLITIS.

clear conception of the anatomical arrangement of the parts is
necessary.

If the reader will refer to Fig. 38 he will see that the lamina
cribrosa is covered by the nearly transparent nerve fibres, which
contain a considerable number of minute blood vessels. These
vessels are derived chiefly from branches of the central artery, but
the plexus is reinforced by twigs from the arterial circle formed by
branches of the posterior ciliary arteries.

The head of the optic nerve, or that part which lies anterior to
the lamina cribrosa, although nearly transparent, is not perfectly

Fig. 38. — Section through optic nerve and papilla.

so, owing to the large number of blood vessels that it contains. Its
transparency varies in different eyes, and while it always allows a
certain amount of white light to be reflected from the lamina, it is
never sufficient to permit the details of that structure to be seen
through it. The floor of a physiological cup forms an apparent
exception, but it must be remembered that this is covered only by
a thin layer of nerve tissue.

The more transparent, therefore, the nerve tissue, the brighter

PHYSIOLOGICAL VARIATIONS OF DISC

11 7

the colour of the disc. The transparency is usually greatest in
light fundi, and in these we may see discs that present all
gradations in colour, from a pale rose to a white but faintly tinged
with red.

In dark fundi, on the other hand, the nerve tissue is usually
less transparent, and we may then get grades of colour from a deep
rich red (as in Plate III., Fig. 6) to a dusky, dirty-looking red,
which appears to be mixed with grey. The latter colour, however,
is seldom met with, except in connection with other congenital
peculiarities of the disc — e.g., opaque nerve fibres (Plate XIII.,
Figs. 36 and 37), congenital crescent (Plate VIII., Fig. 22), or
exaggerated connective tissue ring (Plate V., Fig. 14). In some
dark fundi, on the other hand, the disc looks pale by contrast.

Not only does the colour of the disc differ much in different
eyes, but it is not uniform throughout. For a detailed description
of the appearances which may be presented by different parts of the
disc, the reader is referred to the anatomical description. It is
sufficient here to point out — first, that the outer half of the disc
is often paler than the inner, because the layer of nerve fibres
is there thinner ; and, secondly, that in the part occupied by
the physiological cup there is an entire absence of vascularity,
and the lamina cribrosa is seen as a white surface mottled with
grey.

The margin of the disc, also, presents considerable variations,
according to the extent to which it is softened by the passage over
it of the nerve fibres. These are most abundant at the upper and
lower borders of the disc, so that the edge usually appears softer in
these situations than elsewhere. In addition to this, the margin is
more or less softened, according to the amount of light reflected
from the surface of the fibres. Consequently, while it never
presents so hard a line in the normal condition as in advanced
atrophy, it may yet vary from a fairly sharp line to one that is
rather indistinctly seen as through a transparent film. (Compare
Figures on Plates I., II., and III., with Plate XXXII., Fig. 73).

118

OPTIC NEURITIS OR PAPILLITIS.

These physiological variations in the colour of the disc, and in
the sharpness of its outline, have been fully dealt with in the
first part of this work, because, from their existence not being
sufficiently borne in mind, a pathological condition has often been
erroneously supposed to be present in perfectly normal eyes.

The earliest effect of inflammatory or oedematous conditions of
the head of the nerve, is to impair the transparency of its tissue.
As a result of this, the margin of the disc becomes less distinct,
while its surface appears duller, owing to some loss of light reflex
from the lamina ; for the same reason it seems redder, even when
there is no actual hyperaemia.

A similar appearance is produced by slight turbidity of the
vitreous, due to the presence of fine dust-like opacities in its
anterior part. To avoid overlooking these opacities, careful search
must be made with a convex lens behind the ophthalmoscope,
and a feeble illumination. The plane mirror will also be found of
advantage in doubtful cases.

Blurring from imperfect focussing during the examination, as
in uncorrected myopia, could only be mistaken for commencing
neuritis by a careless observer. But the hypermetropic disc,
described on p. 41, may simulate optic neuritis so closely that the
distinction cannot be made with the ophthalmoscope alone. The
diagnosis must then rest upon the presence of hypermetropia, the
state of the vision, and the progress of the case.

The state of the vision may be of little assistance in
distinguishing optic neuritis from other conditions. The turbidity
of the nerve fibres does not interfere with their function of
conducting impressions from the retina to the brain. Hence
even marked papillitis may coexist with normal vision, a fact
first pointed out by Hughlings Jackson.

Distension of the retinal veins is a sign of papillitis which
commonly makes its appearance soon after the blurring of the
disc margin, although it sometimes precedes it. The distension is
mechanical, and due to obstruction to the return of blood through

VENOUS DISTENSION.

119

the central vein. It is characterised not only by increased breadth
of the veins, but also by their elongation, so that they become
abnormally tortuous, and present an appearance that has been
appropriately designated “snake-like” (see Plate XXXI.).

The distension becomes more marked as the vessels are traced
from the periphery towards the disc. It is often greatest just
before the vessel dips into the substance of the head of the nerve.
At this point the distended vessel may undergo a rather sudden
reduction in size, and may in consequence present an appearance
not unlike an engorged leech.

In pronounced cases, the sinuosities of the vein occur not only
in the plane of the retina, but also perpendicularly to it. When
this is the case, some segments of the vein appear darker than
others, because the column of blood in them is seen “ end on,”
as it were, and the vessel may appear broken in places owing to
its dipping into the substance of the swollen retina (Plate XXXIII.,
Fig. 75; Plate XXXIV., Figs. 76 and 77; and Plate XXXVI.,
Fig. 81).

Distended veins usually appear dark in colour ; this is in
part due to a greater thickness of blood being looked through, and
in part to the retarded current taking up more effete products, so
that the venous character of the blood is exaggerated.

Swelling of the head of the nerve is another important sign of
optic neuritis. It was present in a marked degree in the cases
from which Plate XXXI., Fig. 69 ; Plate XXXII., Fig. 70, and
others, were taken, and is indicated in the pictures by the bold
curves made by the veins as they pass on to the disc. No drawing,
however, can adequately represent the ophthalmoscopic effects
produced by differences in level. These depend on two chief
causes, — the parallactic displacement that occurs when the head is
moved, and the impossibility of accurately focussing at the same
time points which are on different levels. The parallactic
movement may be seen either with the direct or with the indirect
method of examination. With the direct method, the parts that

120

OPTIC NEURITIS OR PAPILLITIS.

are nearest the examiner move in the opposite direction to his
head ; with the indirect, the whole image moves with the lens, but
the nearer parts move more than the distant. Differences in focus
can only be recognised by the direct method. The strongest convex
lens with which the summit of the prominence can be distinctly
seen gives a clue to the extent to which it projects, each
dioptre of refraction corresponding to 0'3 mm. of level. It is
usual to take some object, such as a vessel or band of lymph in
the most prominent part of the disc, and to gauge the swelling
from this. It is evident, however, that other factors have to be
considered in estimating the intensity of the papillitis, such as the
superficial extent of the swelling, the number of new vessels,
haemorrhages, &c.

Hyperaemia and congestion of the disc are frequently present,
and may cause it to appear of the same colour as the fundus. If
its margin is at the same time indistinguishable, the meeting of
the retinal vessels may be the only guide to the position of the
disc. The existence of venous congestion is inferred from the fact
that the retinal veins show signs of stasis. Active hyperaemia
from dilatation of the smaller arteries and capillaries may also be
present, and may bring into view arterial twigs which, in the
normal condition, are too minute to be visible, and may even cause
new vessels to develop (Plate XXXVI., Fig. 81). The hyperaemia
is confined to the disc ; the retinal arteries remain unchanged, or
may even be diminished in size.

Congestion can seldom be diagnosed by the colour of the disc
alone, since such great variations may exist within physiological
limits. But the increased vascularity of the nerve tissue impairs
its transparency, and renders the disc margin less distinct.
Redness, unaccompanied by blurring of the margin, must not be
considered as pathological, unless it is known to be of recent
origin.

It will be evident from what has been said, that, although
no difficulty can arise in recognising fully developed papillitis,

CHOKED DISC AND DESCENDING NEURITIS.

121

the case is different in the early stage. Indeed, when only slight
blurring of the disc margin, and slight redness of its surface
are present, it may be difficult, or even impossible, to be certain
whether we have to deal with a physiological or a pathological
condition. The latter in the early stage is frequently confined
to one eye, or is more advanced in one than in the other, but
exceptions are so numerous that the rule is not of much
practical value. Failure of vision proportionate to the visible
change is strong evidence that the condition is pathological.
On the other hand, retention of normal vision by no means
excludes pathological change. Much more important is the
fact that physiological conditions are stationary, while those
which are pathological tend either to resolve or to become
aggravated, so that any remaining doubt will be dissipated by
the lapse of time.

It was formerly held that there were two varieties of optic
neuritis, which contrasted with each other in respect both of
their mode of causation and their ophthalmoscopic appearance.
The one, presenting great swelling of the disc, and all the signs
of venous obstruction, was called choked disc — a term which
corresponds to the “ Stcmungspapille” of the Germans. The other
form, showing blurring of the disc margin but less swelling and
no signs of venous obstruction, was called descending neuritis.

The so-called choked disc was believed to be produced
by retardation of the current in the central vein, either by
blocking of the cavernous sinus, or by pressure from fluid in
the nerve sheath. In either case the swelling of the head
of the nerve was thought to be aggravated by the unyielding
scleral ring. We now know that complete obliteration of the
cavernous sinus may take place without any ophthalmoscopic
signs, owing to free anastomosis between the orbital and facial
veins at the angle of the orbit. Moreover, when venous
obstruction does exist, independently of inflammation of the
nerve-head, the changes that occur are not identical with those
16

122

OPTIC NEURITIS OR PAPILLITIS.

included under the term choked disc. Pathological evidence,
also, is against the theory of venous obstruction behind the
globe, or of compression exercised by the scleral opening.
Gowers states that he has never, in pathological specimens, seen
signs of compression behind the lamina cribrosa or by the scleral
ring. He considers that the venous obstruction is secondary to
inflammatory changes in the disc, and that the pressure is
exercised by the inflammatory products within the nerve-head,
a view which has been confirmed by other observers.

On the other hand, we must not lose sight of the clinical fact,
whatever be its pathological explanation, that in many cases,
dilatation of the retinal veins precedes the other signs of neuritis.

Ulrich 1 examined post-mortem three cases of cerebral tumour, in
which optic neuritis had developed only a few days before death.
He found oedema of the nerve trunk, apparently an extension of a
similar condition from the brain substance, and compression of the
central vessels within the trunk of the nerve. Such a condition,
however, is certainly exceptional.

Deutschmann 2 holds that the so-called choked disc has no
connection with obstruction from pressure, but that it results from
irritating particles in the cerebro-spinal fluid carried down the
nerve sheaths, and mechanically arrested at their distal extremities
— a view identical with that advanced by Leber at the International
Medical Congress in 1881. Deutschmann arrives at this con-
clusion from the fact that examination of pathological material
shows that compression of the vessels, when present, is always
anterior to the lamina cribrosa, and secondary to exudation into
the head of the nerve, and is, therefore, a result, and not the cause
of the swollen disc. Also, that when the central vein is really
obstructed, as by a thrombus, the symptoms are very different
from those which are presented by the so-called choked disc. The
retinal veins are, indeed, distended and tortuous, but the disc does

1 Arch. f. Ojohth., Leipzig, bd. xviii., p. 53.

2 “ Ueber Neuritis optica und Gehirn-Affectionen,” 1887.

NEURO-RETINITIS OR RETINITIS .

123

not become much swollen, and extensive haemorrhages occur —
conditions which are depicted in Plate XXXIV., Figs. 76 and 77,
and which will be described in detail later on.

Experiments on rabbits gave results consistent with Deutsch-
mann’s views. It was found that the intersheath space might be
injected with fluid, almost to the bursting point, without any
effusion taking place into the retina, but that the retinal arteries
became diminished and the veins distended, while haemorrhages
occurred into the retina. On the other hand, when fluid contain-
ing tubercle bacilli was injected, severe optic neuritis was set up.

I would point out in passing that the good results Brudenell
Carter seems to have obtained by incision of the nerve sheath
in cases of optic neuritis, are cpiite as consistent with the theory
that the fluid contains deleterious particles, as with that which
attributes the neuritis to its mechanical pressure. It is obvious
that an operation of this kind must so modify all the conditions
present that its action might be explained in several ways.

It follows from what has been said that the term choked
disc can no longer be employed to express the result of a distinct
pathological process, but it may be retained as descriptive of a
particular grouping of the ophthalmoscopic signs of papillitis.

Optic neuritis, or neuro-retinitis, may be due to various con-
ditions, which may be conveniently classified under the three
heads — local, intracranial, and general. In the cases that depend
upon a local cause, the affection is monocular, while in those which
result from intracranial or general conditions, both eyes are
eventually affected. Even in these latter cases, however, it is
common for one eye to be attacked before the other, so that the
fact of the condition being monocular at the moment of examina-
tion is not conclusive evidence in favour of a local cause.

The following table shows the different conditions which are
generally recognised as capable of setting up neuritis or neuro-
retinitis ; isolated cases have, however, been recorded, which
were thought to be due to other causes, and it is possible that

124

OPTIC NEURITIS OR PAPILLITIS.

Local Causes.

anything capable of causing peripheral neuritis may occasionally
affect the optic nerves.

j" Cellulitis of orbit.

I Periostitis „

j Wounds „

Tumours „

Thrombosis of the orbital veins and their
tributaries, especially the vena centralis
retinae.

Haemorrhage into the nerve sheath.

Wounds or tumours of the optic nerve.
Wounds of the globe.

Meningitis — a. Traumatic.

,, b. Tubercular.

,, c. Syphilitic.

„ d. Pyaemic, especially from

disease of middle ear.

„ e. Epidemic cerebro-spinal.

Intracranial

Causes.

General

Causes.

Tumour.

Abscess.

Aneurism (especially in the cavernous sinus).
Acute febrile diseases.

Albuminuria.

Influenza.

Anaemia (all forms).

Scurvy.

Diabetes.

Malarial poisoning.

Syphilis.

Poisoning from lead and possibly other
agents.

Leucocythaemia.

Pyaemia.

. Hereditary predisposition.

PAPILLITIS FROM ORBITAL CAUSES.

125

It is evident that several of the causes enumerated above
might act in different ways, and might, therefore, be placed in
either of the three classes, according to circumstances. For
example, syphilis may act as a general cause through the
condition of the blood, thus producing a primary syphilitic
papillitis. This is certainly very rare, and its occurrence is
denied by some authorities. Or it may act as a local cause by
producing a gumma of the nerve or periostitis at the apex of
the orbit ; or, finally, as an intracranial cause by leading to a
gumma of the brain or a gummatous meningitis.

Cases occur from time to time in which optic neuritis is the
only discoverable symptom. Such cannot be classed under any
of the above headings, and the term idiopathic neuritis may,
therefore, be provisionally applied to them pending fuller know-
ledge as to their pathology. These cases are often accompanied
by headache. They are more common in women than in men,
and have been attributed, but often on insufficient evidence, to
cold and suppression of the menses.

Papillitis from Orbital Causes.

Orbital affections may set up papillitis either by pressure
on the nerve, or by direct extension of inflammation to its
structure from the orbital cellular tissue. Wounds of the nerve
immediately produce ophthalmoscopic changes only when they
are situated anterior to the point at which the central vessels
enter the nerve, the appearances then resemble that produced by
thrombosis of the central vein. When the lesion is behind this
point an atrophic process creeps down the nerve, and does not
appear at the disc for several weeks.

Tumours of the optic nerve may cause papillitis, but these cases
are rare. Proptosis and immobility of the eye are prominent
symptoms.

Optic neuritis has sometimes been found in eyes excised on

126

OPTIC NEURITIS OR PAPILLITIS.

account of recent wounds of the front part of the globe, but
opportunities of ophthalmoscopic examination under these circum-
stances can hardly arise.

Optic neuritis occurs in some of the cases which have been
called acute retro-bulbar neuritis. These may conveniently be
considered here, although they form a distinct clinical group.
The characteristic symptom is a very rapid or sudden loss of
vision in one eye, which may be complete. Sometimes this is
preceded or accompanied by tenderness on pressing the eyeball
back into the orbit ; and headache or neuralgia may be present.
The pupil is often dilated, and does not act even to concentrated
light, but its associated movements remain unimpaired. In the
majority of cases vision gradually returns after a few days,
recovery commencing in the periphery of the field, and extending
gradually towards the centre, where a permanent scotoma may
remain. With the return of vision the pupil again becomes
active. Some cases develop a papillitis a few days after the
onset of the symptoms ; others run their course without any
ophthalmoscopic change, a difference which probably depends
upon the situation of the lesion.

Sometimes no recovery of vision occurs, and then optic atrophy
eventually supervenes, whether papillitis has been present or not.

Although both eyes are never affected simultaneously, the
second eye is sometimes attacked after a long interval.

The following cases illustrate some of these points : —

Dr. V., 70, a retired medical man. EE. defective for several years from immature
cataract. V. c + 4 D. = 14 Jaeger.

Had been confined to bed for some weeks with bronchitis. On waking one afternoon
he found that he was quite blind with the LE., which had previously had no defect.
He was unable to see the light of a candle held a few inches away. When seen by the
writer the next morning, there was bare perception of light, and the pupil was inactive.
Ophthalmoscopic examination negative. Two days later he could made out the position of
objects in the room which lay in the periphery of the field. Vision gradually improved,
and in a fortnight he could read DO of Snellen’s reading types, but was unable to see the
middle letters of the longer words. Three months later V = c + 4 I). = 0'3 Snellen, but there
was a minute central scotoma. There was no ophthalmoscopic change throughout.

PAPILLITIS FROM INTRACRANIAL CAUSES.

127

In the following case both eyes seem to have been attacked,
with an interval of a year and eight months : —

Miss C., agecl 22. A nervous excitable woman of distinctly neurotic tendency.

The history of the LE., which was first attacked, is partly compiled from notes kindly
furnished me by Mr. Lawson.

2nd September 1888. — Attacked by severe neuralgia in left temple. The next day this
had gone, but it returned, with less severity, on the third day. On the fourth day, on waking
in the morning, she found that she could not see with the LE. A fortnight later (17th
September) she consulted Mr. Lawson, who found V. RE. f- and 1 Jaeger. LE. letters of
19 J. made out, but unable to see the whole of a letter at a time. OP. muddy-looking,
margin hazy. Two days later (19th September) she was seen by the writer. She still
complained of much dimness in LE, but Y. was found to be (j-. There was very slight
blurring of the disc margin. Not seen again for two years, she then stated that the LE.
recovered completely a few days after her last visit.

7/A May 1890. — Seen on account of failure of RE. She stated that for several days
she had had pain over the right brow. Three days ago (4th May) Y. of RE. failed rapidly,
and continued to get worse till the day before her visit. When seen (7th May) LjE. V. •£
RE. 19 J. letters only. ATisual field normal. Disc margin thought to be a trifle hazy.
Decided tenderness on pressing the globe back into the orbit.

10/A May. — Y. worse. Could see the black and white of 19 J., but could make out no
letters, and could not count fingers. V.F. normal in extent. The test-object occasionally
lost, but no definite scotoma could be mapped out. OP. margin decidedly blurred. No
swelling. No distension of veins. Small vessels on OP. seen quite clearly. Mercurial pill
twice a day.

11 th May. — Disc margin more blurred. Veins engorged.

12/A May. — Disc margin indistinguishable. Veins to arteries as five to two. Very
slight swelling of disc. Y. improved. Counts fingers at 12 in.

13/A May. — V. fingers at 18 in. Disc margin a little clearer.

14/A May. — Patient says that the cloud which has covered the whole field had lifted
at the edges. She could make out the position of objects in the room which lay in the
periphery parts of the field, but was unable to see the light of the fire when looking
straight at it. Is taking the mercury, and is kept in a dark room. Ophthalmoscopic
appearances unaltered.

2nd June. — There has been steady improvement. V. = letters of 10 J. Lateral margins
of disc quite clear. Still cloudy above and below. Colour of disc pale. To take mercury
in small doses, and iron.

7/A June. — V. T6g- and 1 J. puzzled out.

3rd July. — V. f- c — 0. 5 OP. £ one letter. Disc nearly normal in appearance. Not
seen again.

Papillitis from Intracranial Causes.

The anatomical connections of the optic nerves explain
the mode of action of some of the intracranial causes of optic

128

OPTIC NEURITIS OR PAPILLITIS.

neuritis. The prolongation of the cerebral meninges into the
sheaths of the nerve favours direct extension of the inflammation
in meningitis. The continuity of the subarachnoid and the
intervaginal spaces, allows changes in the quantity and quality
of the cerebro-spinal fluid to produce corresponding changes in
the contents of the nerve sheaths. Formerly it was held that the
mere distension of the latter produced optic neuritis mechanically
by pressure on the nerve, and strangulation of its tissues. As
already pointed out, it is more than doubtful whether papillitis
can be produced in this way. But there can be no doubt
that if the fluid contain irritating substances, these may set up
inflammatory changes in the nerve-head. Optic neuritis may
also be caused by inflammation spreading from the brain along the
optic nerve by continuity of tissue. It was formerly thought that
this descending neuritis produced ophthalmoscopic appearances
which could be distinguished from the condition which was
believed to be due to excess of fluid in the sheaths, and which was
known as choked disc. It is now agreed on all hands that this
distinction cannot be made, and the best authorities consider that
most instances of papillitis, resulting from intracranial conditions,
are really examples of descending neuritis.

Next to meningitis, the most frequent intracranial cause of
optic neuritis is tumour. It is probable that the large majority
of cases of intracranial tumour cause papillitis at some stage, but,
as it may be transient, and unaccompanied by any impairment of
vision, it may sometimes escape notice.

Both discs are nearly always affected, although one may be
attacked in advance of the other. When papillitis is present in
one eye only, in a case of intracranial tumour, the fact does not
assist in determining the side of the brain on which the growth is
situated, since the results of post-mortem examination have shown
that the affected eye is on the same and on the opposite side in
nearly equal proportions. The liability to papillitis does not
appear to depend upon the nature or size of the growth, and the

PAPILLITIS FROM GENERAL CAUSES.

129

character of the connection between the intracranial and ocular
conditions is still doubtful. The balance of opinion seems at
present to incline to the belief that the papillitis results from a
direct extension of inflammation along the nerve tissue, although
the special liability of cerebellar tumours to excite it, hardly
supports this view.

The existence of binocular papillitis may, therefore, materially
strengthen the diagnosis of cerebral tumour. But it has per se no
localising value, for, although it is more often due to cerebellar,
than to other, tumours, it may result from a neoplasm situated
in any part of the brain.

Cases of optic neuritis, accompanied by persistent dropping
of clear fluid from the nose, have been observed.1 Frontal
pain and cerebral symptoms of some kind appear always
to be present. It is probable that the fluid comes from the
subarachnoid space, although analysis has not yet proved
conclusively that it is cerebro-spinal fluid.

Papillitis from General Causes.

General conditions may act on the optic nerves in many
different ways. In acute febrile diseases, it is probable that the
papillitis is in many instances directly caused by meningitis. But
it has occurred in cases in which there has been no other reason
to suspect any cerebral complication. An instance of this has
been recorded by Stephenson.2 In this case, well marked double
optic neuritis, with impairment of vision, followed a mild attack
of measles. Optic neuritis may occur in the course of any of
the specific fevers, but is said to do so with especial frequency
in typhus. In the case from which Plate XXXVI., Fig. 81, was
taken, enteric fever was probably the cause of the neuritis,

1 Nettleship, Ophth. Rev., London, vol. ii., p. 1 : Priestley Smith, ibid. ; and Leber, Arch. .
Ophth. and Otol., N. Y., vol. xxix., p. 271.

2 Trans. Ophth. Soc., vol. viii., p. 250.

130

OPTIC NEURITIS OR PAPILLITIS.

although the patient had also suffered from disease of the
middle ear.

Many general diseases would seem to produce neuritis by
causing changes in the composition of the blood. This mode of
action is obvious, for example, in leucocythaemia. In this disease
the immense increase in the number of white corpuscles impedes
the circulation through the small vessels of the retina. In anaemia
and scurvy, also, the character of the blood has no doubt a direct
influence in causing neuro-retinitis, by allowing fluid to transude
more readily through the walls of the capillaries. There are other
general morbid conditions, attended by great alterations in the
blood, in which the mode of production of the neuritis is not so
obvious ; as examples — diabetes, lead poisoning, and albuminuria
may be cited. In these it is probable that other conditions (besides
the state of the blood) contribute to the result. For instance, in
albuminuria, besides the fact that the blood is highly charged with
nitrogenous compounds, we have to take into consideration the
changes in the walls of the blood vessels, and the hypertrophy of
the left ventricle of the heart.

The ophthalmoscopic appearances of optic neuritis vary in
different cases, as will be evident by comparing the several
figures in the Atlas. These variations depend chiefly upon the
severity and stage of the inflammation, and on the degree to
which the retina is involved, but only to a comparatively slight
extent on the cause of the condition. Neuritis from intracranial
affections and from Bright’s disease are, however, types of two very
different classes. In neuritis from intracranial conditions, the
changes are either confined to the disc or are most marked there ;
the retina is affected, if at all, secondarily, and late in the disease ;
and haemorrhages are the exception rather than the rule (Plate
XXXI., Figs. 67 and 69, may be instanced as examples). The disc is
much swollen, its margin indistinct or invisible, the veins engorged
and tortuous. In albuminuric retinitis, on the other hand, there
are numerous retinal haemorrhages, large soft woolly looking

PAPILLITIS FROM GENERAL CAUSES.

131

patches of effusion, and some glistening white dots ; the disc
margin may be blurred or invisible, but the swelling of the disc
is inconsiderable (see Plate XXXVI., Figs. 82 and 84). This
distinction cannot, however, always be made, indeed, the con-
ditions may be reversed ; hence it is impossible to diagnose the
cause of the neuritis by the ophthalmoscope alone.

Papillitis may subside completely ; the inflammatory products
may undergo a partial organisation into connective tissue ; or
the disc may pass into a state of atrophy.

The inflammatory products in the retina show no tendency
to organise, or to break down into pus. On the contrary,
when the neuritis subsides, they are generally absorbed, but
they may produce permanent degenerative changes in the
retina.

When neuritis begins to subside (as in Plate XXXI., Fig. 66),
the nerve-head becomes paler and the swelling diminishes.
Gradually the margin of the disc clears, generally first on the
temporal side. The tortuosity of the vessels persists longer, and
if it has been very great, may never subside. The vessels are
often accompanied on the disc, and for a short distance beyond
it, by fine white lines. These are due to effusion into, or

changes in, the sheath of the vessels (Plate XXXI., Fig. 67).
Sometimes these lines remain permanently, and then afford
important evidence of the previous existence of neuritis. It
must not be forgotten, however, that a similar appearance is
produced by the bands of connective tissue that are not uncommon
as a congenital condition.

If the inflammatory material effused into the head of the
nerve undergoes organisation, the disc will remain of a whiter
colour than normal, and its margin may be blurred and irregular.
It is important to note that these conditions may exist with
normal vision. As a rule, however, persistent pallor following
neuritis indicates that some of the nerve fibres in the disc have
become atrophied. When this is the case the vision is subnormal,

132

OPTIC NEURITIS OR PAPILLITIS.

and the visual field is usually contracted. Although such a partial
atrophy is necessarily permanent, it need not be progressive. It
is due to the nerve fibres having been subjected to so much
compression that they are unable to recover even when the
pressure is removed.

CHAPTER VIII.

NEURO-RETINITIS AND RETINITIS.

So far we have chiefly dealt with the changes that occur
in the disc itself, and are included under the term papillitis ;
we now pass on to consider those cases in which the retina
also is affected — neuro-retinitis. The venous obstruction may

mechanically induce changes in the retina. As the pressure
in the capillaries becomes greater, haemorrhages occur into its
substance. These, as well as haemorrhages from other causes,
will be considered in detail later on. Meanwhile other retinal
changes may occur. These are chiefly of two kinds — (a) soft-edged,
woolly-looking patches, round, oval, or kidney-shaped, varying in
size, but having an average diameter equal to half that of the disc
(Plate XXXVI., Fig. 81, and Plate XXXVII., Fig. 82) ; (b) small,
more brilliant and harder looking dots, the larger ones about the
diameter of the primary retinal vessels, others much smaller.
These usually appear at a later stage than the woolly patches
(Plate XXXVI, Figs. 80, 81, Plate XXXVII, Fig. 82, and
Plate XXXVIII, Fig. 87), except in the yellow spot region,
where they are sometimes seen soon after the onset of the
inflammation. In this situation they tend to arrange themselves
in lines radiating from a centre, as shown in Plate XXXVII,
Fig. 84, and to a less degree in other figures.

Our present knowledge points to the conclusion that identical
ophthalmoscopic appearances may be due to different pathological
conditions. Thus the microscope shows that the larger patches
described under (a) may be due to varicose swellings of the nerve
fibres, to cellular exudation (the cells being derived either from
the white corpuscles of the blood, or from the nuclear layer of

134

NEURO-RETINITIS AND RETINITIS.

the retina), or to fibrinous exudation which coagulates between
the nerve fibres. Fat globules are usually found associated with
all these conditions, and are derived both from the breaking
down of the retinal elements, and from degeneration of the effused
products of inflammation. The small chalky dots (b) are probably
generally due to changes in the fibres of Muller.

Neuro-retinitis is not unfrequently accompanied by wavy
swelling of the retina, as indicated by tortuosity of the vessels,
the curves of which are perpendicular to the normal plane of
the retina. More rarely the surface is thrown into regular
parallel ridges, like those left on the sand by the receding tide.
An example of this is shown in Plate XXXII., Fig. 70.
Nettleship1 has recorded a case, which, judging from the excellent
chromo-lithograph that accompanies the description, is of the
same nature. He, however, attributes the lines in his case to
imperfect subsidence of choroidal oedema. But the similarity of
the lines to the ridges of a detached retina, and the association
with neuro-retinitis seem rather to point to a retinal origin.
It is not improbable that oedema of the choroid does occur in
neuro-retinitis, but the free anastomosis of the choroidal vessels
is not favourable to its sharp limitation.

The changes in the retina, like those in the disc, may proceed
either to resolution or to degeneration of tissue.

Even very extensive retinitis may recover. Thus, the woolly
patches may be absorbed completely, and haemorrhages may
be converted into white patches, which eventually disappear
(Plate XXXV., Fig. 78, and Plate XXXVII., Fig. 83). The
most persistent lesions are the fine chalky dots, which are most
numerous at the macula, but also occur in other parts of the
retina. Even these, however, may completely disappear. For
example, in the case from which Plate XXXV., Fig. 78, was
drawn, only a very few small white dots remained in the
neighbourhood of the macula some months later. On the other

1 Trans. Ophth. Soc., vol. iv., p. 167.

NEURO-RETINITIS AND RETINITIS.

135

hand, extensive exudation in the macular region sometimes
produces permanent scarring, such as is seen in Plate XXI Y.,
Fig. 57. That the retina does not more often recover from the
results of inflammation is due to the fact that the cause of the
inflammation is generally persistent. When it is transient, as in
the albuminuria of pregnancy, recovery from very extensive
retinitis is not uncommon.

When degenerative changes ensue, the soft woolly patches are
replaced by smaller flat-looking areas, with well-defined but
irregular outlines. These have a brilliant, sometimes almost a
metallic lustre, which it is difficult to depict satisfactorily.
Occasionally, the surface of the patches looks irregular, as if
composed of a crystalline sub-
stance. That this is really
the case seems probable, from
the fact that prismatic colours
can now and then be seen.

Such crystals probably consist
of cholesterine. The scarring
at the macula referred to
above (Plate XXIV., Fig. 57)
must also be looked upon as
a degenerative change.

Allusion has been made
to the stellate arrangement that retinal effusions tend to
assume when situated in the region of the macula. This
appearance is well seen in Plate XXXVII., Fig. 84, and to a
lesser degree in Plate XXXV., Fig. 78, and Plate XXXVI.,
Fig. 80. This characteristic grouping is due to the anatomical
distribution of the fibrillar elements of the retina, and particularly
of the fibres of Muller at this part, already described on page 64,
and shown in Fig. 39. It will be noted that at the actual centre
the fibres are vertical, and this corresponds with the fact that the
radiating lines stop short before reaching the centre.

Fig. 39. — Section through the macula. (After
Golding Bird and Schafer.)

136

NEURO-RETINITIS AND RETINITIS.

This explanation of the production of the star-figure is
not universally accepted. Thus, Marcus Gunn1 attributes it to
cedematous swelling. This tends to stretch the retina in all
directions, but the stretching is resisted at the macula by adhesion
between the retina and the choroid. Consequently the retina is
thrown into radiating folds, much in the same way as would
happen if an attempt were made to draw the centre of a sheet
through a ring. Degenerative changes occurring along the lines
of creasing would account for the star-figure persisting after the
subsidence of the swelling.

The stellate arrangement is not confined to such changes as are
obviously inflammatory or degenerative in character. A case
which does not seem to belong to either of these categories is
shown in Plate XXXVIII., Fig. 85. The patient was young,
and apparently in good health. The loss of vision was rapid, if not
sudden, and preceded the appearance of the changes at the
macula by eight or eleven days. Considering how conspicuous
those changes were, they proved somewhat evanescent, for in
thirty-two days they had in great measure disappeared (as shown
in Plate XXXVIII., Fig. 86). The history of the case seems most
consistent with some interference with the circulation, inducing
secondary changes, possibly of the nature of oedematous effusion,
in the retina at this part ; but the appearances are, it must be
admitted, quite unlike those met with in embolism of the central
artery, for in such cases the whole retina becomes opaque, and
although at a later stage the changes become limited to the
macular region, they do not even then assume the star-like form.

The two following cases seem to be examples of the condition
just described : —

A woman, aged 33 (Dahrenstadt, Centralbl. f jprakt. Augenli., Leipzig, February, 1892),
had had pain over the left eye for three months, but the sight had only failed two days
before her visit. When seen Y. was A:V> and a sector-like defect was present in the lower
and inner quadrant of the field. There was some blurring of the disc margin, and a

Trans. 8th Internat. Ophfh. Congress , Edinburgh, 1894.

ALBUMINURIC RETINITIS.

137

patch of retinal effusion close to it above. In this situation the veins were somewhat
distended and tortuous. At the macula was a stellate figure, consisting of about fifty lines
radiating from near the centre ; the lines diminished in size towards their peripheral
extremities, and appeared to be composed of numerous dots. The diagnosis made was
thrombosis of the superior temporal artery. Treatment by iodide of potassium, mercurial
inunctions, and massage, was followed on the second day by improvement. The superior
temporal artery eventually became converted into a fine red streak, bounded by white
lines, and the star-like figure gradually disappeared till scarcely a trace of it remained.
There was no history of syphilis, and albumen was not present in the urine.

Frail L., aged 59 (Hirschberg, CentralU. f. prakt. Augenh., Leipzig, 1882, p. 330).
Three days before visit sudden loss of vision in RE. Arteries atheromatous. Palpitation
without valvular lesion, and haemoptysis without physical signs, were present. Urine
normal.

RE. V. = Ty5 . Visual field normal in extent, a central positive scotoma having a
radius of 8°. Optic disc normal ; between it and the fovea, a large number of extremely
minute white dots, which had an almost crystalline brilliancy. Nine days later, the
scotoma had diminished, but the patient complained of seeing a violet cloud in the centre
of the field. The fovea was seen to be surrounded by a wreath of regularly arranged white
dots, and similar dots were thickly crowded between the disc and the fovea,

A month later these dots had arranged themselves into fine lines, radiating from the
disc ; in another month, there was in this situation a star-like figure with fifteen rays,
while between the US', and the disc were four rays, arranged like the letter X. Nine
months after the first visit, the fundus was normal.

A somewhat similar case has been published by Mr. Hartridge (Trans. Ophth. Soc.,
vol. ix., p. 144), with a chromo-lithograph, in which the changes were noticed after a blow
on the eye.

The following varieties of retinitis are of sufficient importance
to be dealt with separately : —

Albuminuric Retinitis.

Nephritic, or albuminuric retinitis, may occur in any form of
renal disease, but is most commonly associated with the contracted
granular kidney. The disease, as far as its ophthalmoscopic
appearances are concerned, is met with in two forms, which may
conveniently be called acute and chronic, corresponding respectively
to the inflammatory and degenerative varieties of Gowers.1 The
acute form is characterised by large areas of retinal effusion, by
haemorrhages, and by much blurring of the disc margin ; the

1 “ Medical Ophthalmoscopy.

138

NEURO-RETINITIS AND RETINITIS.

chronic by smaller retinal spots of brilliant white colour. At
a later stage these latter are replaced by flat-looking glistening
spots of slightly larger size and of irregular shape, or by large
glistening areas formed by coalescence of the smaller dots.
On the surface of these, glistening crystalline-looking bodies of
minute size can sometimes be seen ; these are probably crystals of
cholesterine. On several occasions the writer has seen prismatic
colours in such bodies. There is often an irregular deposit of
pigment over these old patches. Haemorrhages are generally
absent or few in number, and the disc may be unaffected. The
chronic may represent the late stage of the acute variety, or may
occur independently.

The soft woolly patches (such as those seen in Plate XXXVIT.,
Fig. 82) may be due to several pathological conditions which
frequently coexist ; as, for example, effusion of fluid among the
nerve fibres, exudation of leucocytes, and varicose swellings on the
nerve fibres. The smaller, more glistening dots, seen in the same
picture, are caused by fatty degeneration either of effused products
or of the tissue of the retina. When situated at the macula thev
tend to assume the spoke-like arrangement shown in Plate
XXXVII., Fig. 84.

In many cases lymph is exuded into the perivascular sheaths ;
the vessels are then seen to be bordered by white lines, or they
may in places be entirely concealed by the effusion, and so
present an appearance of broad white bands. A somewhat similar
appearance may be produced by the vessel wall itself undergoing
degenerative changes which convert it into a band of chalky
whiteness (Plate XL., Fig. 90). According to Brailey and
Edmunds,1 changes in the retinal vessels are to be found with the
microscope in most cases of chronic contracted granular kidneys,
even although the ophthalmoscopic appearances may be normal.
These changes consist in “a general thickening and hyper-
nucleation of the coats of the arteries, without any diminution of

1 Trans. Oplith. Soc., vol i., p. 44.

ALBUMINURIC RETINITIS.

139

their calibre, with a somewhat similar affection of the capillaries.”
In another condition, thought to be a later stage of this, “the
arterial walls are thick and structureless, and the capillaries hyaline
and rigid, standing open on section. In other instances thickening
of the arterial wall both increased the diameter of the vessel and
also narrowed its lumen, in some cases, to complete obliteration.
The arteries in the kidneys in the same patients presented similar
changes.”

Hyaline thickening of the vessel wall does not impair its
transparency. It may, therefore, exist without any ophthalmo-
scopic sign. The condition can sometimes be recognised by the
brilliant, rather glassy appearance presented by the retinal arteries,
(which has been aptly compared to bright copper wire), and by the
light streak being abnormally conspicuous. At the point where
an artery, thickened in this manner, crosses a vein the latter vessel
may appear broken, and the gap to be only partly filled by the
artery (Plate XXXVI., Fig. 80, and Plate XXXVII., Fig. 84).
It would seem that in some cases the thickened artery, by pressing
on the vein, retards the blood current, and causes dilatation of the
vein on the distal side. But in the cases shown, as well as in one
recorded by Marcus Gunn,1 there was no such dilatation ; there-
fore, it is impossible to accept the view that the apparent break
in the vein corresponds with any considerable obstruction of the
blood current, and some other explanation must be sought for the
appearance. We shall consider this subject again when dealing
with changes in the walls of the vessels (see page 160).

Albuminuric retinitis usually occurs only at a late stage of
chronic renal disease ; its presence may, therefore, be taken to
warrant a serious prognosis with regard to length of life. This
view has been confirmed by statistics. Stedman Bull 2 found
that, out of a total of 104 cases of albuminuric retinitis, no fewer
than 85 died within two years of the discovery of the retinal
changes ; while, of the remaining 19, only 4 were under observa-

1 Trans. Ophtli. Soc., vol. xii., p. 124.

2 Trans. Am. Opldh. Soc., 1886, p. 184,

140

NEURO-RETINITIS AND RETINITIS.

tion for more than a year. Miley1 took infinite pains to trace
the career of all the patients who were treated in the London
Hospital for acute and chronic renal disease (exclusive of acute
scarlatinal cases) in the years 1884-5-6. The results are in
accord with Dr. Bull's, but they have the advantage of enabling a
comparison to be made between the renal cases with retinal
complication and those without it, and show that the prognosis in
the former is much more serious than in the latter.

It is doubtful how far these statistics, compiled from hospital
patients, are applicable to those in easier circumstances. Renal
disease is an affection which, above all others, is aggravated by
exposure and want of care. Its deleterious consequences may
be long delayed, on the other hand, by care as to diet and
clothing, choice of climate, vigilant regulation of the excretory
functions, and that attention to the thousand-and-one details of
hygiene and comfort, which is possible only in the case of the
well-to-do.

Although, however, the actual duration of life may be greater
in private patients, it cannot be doubted that albuminuric retinitis
is even in them a grave factor in the prognosis.

The prognosis, with regard to sight, depends chiefly upon the
tendency to haemorrhage and the existence of degenerative changes
at the macula. There is always considerable liability to retinal
haemorrhage in all cases, owing to the pathological state of the
capillaries already described, but cases differ much in this respect.
Extensive changes of a degenerative character in the region of the
macula preclude the recovery of useful vision, and even inflam-
matory exudation there, if at all abundant, is usually followed by
permanent impairment. The disease is progressive, but its course
is so chronic that, unless intercurrent attacks of haemorrhage take
place, the deterioration in the vision is often not much noticed by
the patient.

Uraemic amblyopia may occur independently of any retinal

1 Trans. Ojohth. Soc., vol. viii., p. 132.

DIABETIC RETINITIS.

141

changes, and cause sudden and complete blindness. In such cases
the pupils are usually dilated, and their reaction to light some-
times persists, even though perception of light may be entirely
lost. Rapid and complete recovery follows the elimination of the
poison.

Retinitis resulting from the albuminuria of pregnancy differs
from that due to chronic renal disease. The retinal changes are
of the typical acute form, very large white areas being common.
There is, consequently, considerable impairment of sight. In
spite of this, and of the extensive retinal changes, complete
recovery of vision may take place if the pregnancy terminate
before the retinal tissue has undergone degeneration. It must,
however, be remembered that the retinitis is likely to recur with
each succeeding pregnancy.

Retinitis occasionally results from acute scarlatinal nephritis.
These cases are analogous to the preceding as regards the character
of the retinal disease ; the prognosis is probably less hopeful,
but they are not sufficiently frequent to permit a positive
statement on the subject.

Diabetic Retinitis.

Diabetes is undoubtedly a cause of inflammation of the retina.
The appearances presented by diabetic retinitis have been
described in great detail by many authors.1 Unfortunately, the
descriptions differ much from each other, while they all contain
points of resemblance to the chronic form of albuminuric retinitis.
It would seem, therefore, that there are no ophthalmoscopic signs
which enable us to discriminate with certainty between albumin-
uric and diabetic retinitis.

The cases in which new vessels are formed in the vitreous in
diabetic patients will be mentioned later on.

1 For a summary of the views of various authors ou this subject see Oscar Dodd (Arch. Ophth.
and Otol., N, Y., vol. xxiv., p. 206).

142

NEURO-RETINITIS AND RETINITIS.

Leucocythj5mic Retinitis.

Leucocythsemic retinitis is so closely associated with the
condition of the blood, and is accompanied by such marked
changes in the appearance of the retinal vessels, that its con-
sideration may be conveniently postponed till we come to discuss
affections of the vascular system of the retina.

Retinitis Circinata.

Among the rarer forms of inflammation is that to which the
name of Retinitis Circinata has been given by Professor Fuchs.1

Thy characteristic feature of the condition is the presence of a
belt of white dots (or a white surface formed by their coalescence)
surrounding the macula, and enclosing an oval area of considerable
size ; the white belt usually reaches nearly to the upper and
lower temporal vessels. Its width varies, but it seldom exceeds
half the diameter of the disc, and it may be broken at several
points. Changes at the macula itself are also present.

The band is made up of small white dots of irregular shape ;
these tend to run together, and thus form larger white patches lying
in contact. The retinal vessels pass over their surface unchanged.

Nothing is known of the morbid anatomy of the affection,
which occurs in persons who are well past middle life, and does not
appear to depend upon any recognised general disease. It runs
a very chronic course, the appearances changing but little in the
course of years.

Plastic Retinitis and Cicatricial Changes.

There are some forms of retinitis in which the inflammatory
exudation becomes organised and converted into strands of con-

1 For further details the reader should consult Professor Fuch’s original paper (Arch. f. Oplith.,
Leipzig, vol. xxxix., p. 229), and Holmes Spicer (Trans. Ojphth. Soc., vol. xiv., p. 132).

PLASTIC RETINITIS AND CICATRICIAL CHANGES. 143

nective tissue. In this manner may be explained some of the
tightly stretched bands, or irregularly shaped white membranes
with well-defined hard edges, which are sometimes seen on the
retina. An example of the latter is shown in Plate XXV., Fig. 59,
and of the former in Plate XLV., Fig. 99. These changes may
conveniently be grouped under the term cicatricial, since they
are probably produced by the contraction of new-formed fibrous
tissue. But they may be due to a variety of causes, and it is
not always possible to be certain whether the visible changes
really lie in the retina or in the choroid. The changes at the
macula, following inflammatory exudation (Plate XXIV., Fig.
57), are also probably cicatricial, but are not included in this
section.

The condition depicted in Plate XLV., Fig. 99, is characterised
by the presence of white bands radiating from the disc, which have
the appearance of being tightly stretched. Some of the bands at
their peripheral extremities spread out fan -wise, as if they had
originally been broader, and had shrunk to their present dimensions.
As, however, they lie beneath the retinal vessels, it is difficult
to conceive of any great shrinking having occurred, since the
vessels show no evidence of being displaced. In the case from
which this drawing was made there was a history of syphilis, and
it is probable that all these cases are due to this disease. The
term retinitis proliferans would have been appropriate had it not
been applied by Manz and others to a totally different condition,
in which membranous exudations are formed in front of the retina,

A somewhat similar appearance, as far as the direction of the
bands is concerned, is now and again seen in progressive myopia. In
such cases the lines are not so conspicuous, as they have not such
a brilliant whiteness, as in Plate XLV., Fig. 99, but are more like
those in Plate XXXII., Fig. 70. They are usually most con-
spicuous between the disc and the macula, but they do not extend
far towards the periphery. It is difficult to determine whether they
are situated in the retina or in the choroid, but in either case they

144

NEURO-RETINITIS AND RETINITIS.

probably result from the traction on the tunics. They have some-
times been described as cracks or tears in the choroid, but they
differ so essentially from the ruptures of the choroid with which
we are familiar, that it is difficult to believe that they are of this
nature. Their appearance is sometimes suggestive of ridges in
the retina, but the lack of any evidence that they are raised
above the level of the rest of the retina makes the acceptance
of this explanation equally difficult. It seems more probable
that along the lines of greatest traction the fibrous elements of the
retina become hypertrophied at the expense of its nervous tissue,
and that the resulting bands are analogous to cicatricial tissue.

The more membranous form of cicatricial change shown in Plate
XXV., Fig. 59, has already been referred to as a retinal complication
of advanced choroiditis. Here an irregular glistening white patch
is formed. In the case depicted it is seen to occupy a large area,
and to present numerous round or oval openings, while the border
of the patch presents deep concavities or bays, with hard sharp
edges. This appearance of the border, and the presence of
circular openings, afford a means of distinguishing such a patch
from an area of exposed sclerotic, which it occasionally resembles
in colour.

These membranous patches in the retina are usually the result
of old choroiditis. The retina becomes adherent to the choroid over
the affected area, inflammatory exudation takes place from the
choroid into the retina, and the resulting opacity is partly
inflammatory and partly cicatricial.

It is not often that there is any difficulty in distinguishing
between an area of exposed sclerotic and connective tissue in the
retina. The difference in the shape of the patch in the two
conditions has already been mentioned. The area of choroidal
atrophy is usually bordered by pigment, and the pearly whiteness
of exposed sclerotic is sufficiently characteristic.

The condition which has been described by Manz 1 under the

1 Arch.f. Ophth., Leipzig, bd. xxii., p. 229; and bd. xxvi., p. 55.

PLASTIC RETINITIS AND CICATRICIAL CHANGES. 145

name of retinitis proliferans differs from that which I have
called plastic retinitis in that the membranous formations which
constitute the typical ophthalmoscopic appearance of the affection
lie entirely in front of the retina.

The membranous opacities may arch over the disc in a
tent-like manner, and so conceal it wholly or in part. They

have the appearance of being tightly stretched, as if they
had undergone contraction, and are brilliant white in colour.
Towards the periphery they either spread out fan-wise or
divide into processes which are attached to the fundus. In
other cases the opacity appears to have a preference for following
the course of the vessels, lying, however, well in front of
them.

When there are, at the same time, opacities in the vitreous,
obscuring the view, the condition might be mistaken for detach-
ment of the retina ; but the mistake could hardly occur if a good
view were obtained, as the tightly stretched look of the opacity in
retinitis proliferans is very different from the soft wavy appearance
of a detachment.

Analogous to these cases, and possibly of the same nature, are
those in which brilliant, glistening white bands stretch tightly
across the vitreous from one part of the fundus to another. Many
of them widen out fan-wise towards their attachment, so that they
present the appearance of having become narrowed in the middle
by contraction. Sometimes vessels can be traced some distance
into the bands.

The pathology of retinitis proliferans is at present obscure.
That it is due to direct inflammatory exudation from the retina,
as implied by its name, is hardly consistent with the ophthal-
moscopic appearance, for wherever there are gaps in the
membrane, the fundus appears normal, or nearly so. It is true
that in Manz’s cases changes were found in the retina on
microscopical examination, but there was no evidence of their
direct connection with the membranous opacity.

146

NEURO-RETINITIS AND RETINITIS.

Dr. S. Schultze 1 has given good reasons for believing that this
condition is always the result of haemorrhage into the vitreous.
In most of the published cases there is a history of sudden loss
of sight some years previously, and in Schultze’s two patients this
was known to have been due to this cause.

1 Arch. f. Augenh., Wiesb., bd. xxv.

CHAPTER IX.

OPTIC ATROPHY.

Atrophy of the optic nerve may depend upon a variety of
causes. It may be conveniently considered under the following
heads, viz. : — (1) Post-Neuritic Atrophy ; (2) Simple Atrophy ; (3)
Hereditary Optic Atrophy ; and (4) Secondary Atrophy. Lastly,
Simple Glaucoma will be included.

Post-Neuritic Atrophy.

We saw at the conclusion of Chapter VII. that papillitis may
result in a partial atrophy of the disc which may remain stationary.
The atrophy in other cases is progressive, and the prognosis
is then exceedingly grave, as complete blindness is the usual
result. Increasing pallor of the disc, if accompanied by pro-
gressive impairment of vision, is a sure indication that the nerve
is degenerating. While the pallor of the disc is increasing its
margin becomes clearer, generally first on the temporal side (Plate
XXXII., Fig. 72). When the atrophy is complete, the d’sc will
present a dead white colour, the physiological cup will be filled
up, and the margin, though clearly visible, does not usually
present the hard line characteristic of simple atrophy (Plate
XXXII., Fig. 71).

The foregoing signs of post-neuritic atrophy are illustrated
in Plate XXXII., Fig. 72. The atrophy in this case is not
complete, being more advanced in the outer part of the disc,
which is here of the typical uniform white colour. The
corresponding part of the disc margin is distinct. The inner
half of the disc still shows by its blurred outline the presence of

148

OPTIC ATROPHY.

neuritis. We may contrast with this Plate XXXII., Fig. 73,
which is an example of simple atrophy — that is, atrophy not
preceded by neuritis. The disc margin is here abnormally hard
and sharp, and presents no irregularities. The surface of the disc
is not of the dead white uniform colour, but is bluish or greyish,
and is somewhat mottled from the lamina cribrosa being seen
through the abnormally transparent and wasted tissue. This
mottling is often much more pronounced than in this instance.

This form of atrophy will be considered more fully presently.

The following table may serve to emphasise the main points of
distinction between the post-neuritic and simple forms of
atrophy : —

Post-neuritic Atrophy.

Simple Atrophy ■

Colour of Disc,

Uniform. Dead white.

Stippled. Bluish or greyish

white.

Surface „

Flat. Physiological cup usually
filled in.

May be very slightly concave.
Physiological cup not filled in.

Margin

Not more distinct than normal.
May be blurred in places. Is
often irregular.

Much more distinct than normal.
Not irregular.

Larger Vessels,

Diminished in size. Accompanied
in places by white lines.

Normal.

Simple atrophy never simulates the post-neuritic, but the
latter in an advanced stage may exactly resemble simple atrophy.
This is owing to the products of inflammation being entirely
removed so that the tissue of the nerve head again becomes
transparent, and allows the lamina cribrosa to show through.
This explains the colour of the 'disc in Plate XXXII., Fig. 71,
which is like that of simple atrophy ; although from the history

SIMPLE ATROPHY.

149

of the case, the small size of the arteries, and the white lines
accompanying them, it is certain that the condition was post-
neuritic.

The atrophic changes consecutive to neuritis are not always
limited to the disc. In some cases they invade the adjacent
choroid, so that the disc is encircled by a ring of choroidal
atrophy. In others the pigment layer of the retina becomes
extensively atrophied, as seen in Plate XXIV., Fig. 57, and
Plate XXXII., Fig. 71.

Simple Atrophy.

This is sometimes called primary atrophy, but the term is
open to the objection that in the cases intended to be indicated
by it, the atrophy is, in reality, always secondary to, and a direct
extension of, atrophic changes in the trunk of the optic nerve.
If employed, therefore, it must only be as a contrast to post-
neuritic atrophy, and not as implying that the head of the optic
nerve is the primary seat of disease.

There is a variety of optic atrophy, intermediate between these,
which would, without hesitation, be classed under simple atrophy,
were it not for the circumstance that in the early stage there is
some evidence of neuritis, as shown by a slight and temporary
blurring of the disc margin. This slight neuritis is a concomitant
affection, and evidently not the cause of the atrophy, and the
cases would therefore be correctly classified under simple atrophy.
Some cases of hereditary optic atrophy afford examples of this
condition.

I do not purpose discussing at all fully the various conditions
which may lead to optic atrophy, but only to direct attention to
those which are most common or best known.

The most typical examples of descending atrophy are furnished
by cases in which the conductivity of the optic nerve is completely
destroyed by an injury at some spot between the optic com-

150

OPTIC ATROPHY.

missure and the point of entry into the nerve of the central
vessels. Immediate and total blindness of the corresponding eye
results, but no visible change occurs in the disc till about three
weeks later, the exact date depending on the seat of the lesion,
and possibly varying also, but to a less degree, in different
individuals. Progressive pallor of the disc, without alteration
in the size of the vessels then appears, and it increases till the
disc assumes the appearance characteristic of complete simple
atrophy. The injury in these cases may be either a penetrating
wound of the orbit, or a blow on the head, usually in the frontal
region.

When, on the other hand, the lesion affects a part of the
nerve that contains the central vessels, conspicuous changes
immediately make their appearance in the fundus. The most
marked of these are diminution in the size of the arteries and
extensive haemorrhages. The fundus presenting an appearance
resembling that caused by thrombosis of the central vein.

The gravity of the injury in punctured wounds of the orbit
is often overlooked, owing to the external opening being small.
In these cases it is not uncommon for other orbital nerves to be
injured at the same time. Optic atrophy following severe blows
has in former times been classed as reflex amblyopia ; but
there can be little doubt that the lesion which destroys vision is
a fracture passing across the optic foramen. Holder 1 has shown
that this foramen is implicated in 60 per cent, of fractures of the
skull.

Periosteal thickening from rheumatism or syphilis may bring
about the same result more gradually. In such cases the more
diffuse character of the lesion, as compared with that due to
injury, is likely to lead to simultaneous implication of the nerves
passing through the sphenoidal fissure.

Pressure on the optic commissure may cause simple atrophy
in both eyes, hi- temporal hemianopsia accompanying the

1 Quoted by Snell, Trans. Ophth. Sue., vol. xi., p. 13G.

SIMPLE ATROPHY.

151

failure of vision. Distension of the third ventricle in internal
hydrocephalus is said by Gowers frequently to act in this
manner. The loss of sight that occurs in acromegaly is believed
to be due to pressure exerted on the commissure by the enlarged
pitnitary body.

Sclerosis of the spinal cord or brain is not unfrequently
accompanied by similar changes in the optic nerves, which cause
impairment of vision, and, later on, atrophy of the discs.

The particular form of optic atrophy which most frequently
comes under the notice of the ophthalmic surgeon is that resulting
from posterior sclerosis (locomotor ataxy). This would seem to
be due not so much to the relative frequency of dorsal, as com-
pared with other forms of sclerosis, as to the fact that in it vision
is affected early, before the general symptoms have led the patient
to seek the aid of the physician.

It is obvious that the relative frequency of the various forms
of disease of the nervous system as causes of optic atrophy, must
be ascertained from general, and not from ophthalmic, cliniques.
A statistical inquiry in this direction by Uhthoff 1 showed that
optic atrophy occurred in 45 per cent, of cases of disseminated
sclerosis, in 18 per cent, of locomotor ataxy, and in 7 per cent, of
general paralysis.

Disseminated sclerosis being such a frequent cause of optic
atrophy, it becomes important to follow UhthofFs conclusions a
little further, the more so as the symptoms in many cases closely
resemble those of tobacco amblyopia.

A marked feature is the want of correspondence between the
ophthalmoscopic changes and the vision. Thus, out of 100 cases
(excluding 7 in which there were opacities of the media), there
was pronounced optic atrophy in 3 ; in all these vision was bad.
Thirty-seven cases showed various degrees of pallor of the disc ;
vision was affected in 23 of these, but unaffected in the other 14.

1 “Die bei multiplen Herdsklerose vorkommenden Augenstorungen,” 1889. (A good abstract
in Ophth. Rev., London, vol. ix., p. 1.)

152

OPTIC ATROPHY.

Optic neuritis was present in 5 cases ; vision being affected in 4,
and unaffected in 1. The ophthalmoscopic appearances were
normal in 48, only 5 of these had bad vision, while in the
remaining 43 it was unaffected.

As to the visual field, a central scotoma (without any general
limitation) was the most common condition found. This obser-
vation is important, inasmuch as the existence of a central scotoma
in a smoker might easily lead to a diagnosis of tobacco amblyopia
— a mistake the more likely to occur if (as sometimes happens in
disseminated sclerosis) the ocular should precede the general
symptoms by a considerable interval of time. For many other
interesting points, we must refer the reader to Dr. UhthofFs
original paper.

The ophthalmoscopic appearance characteristic of simple
atrophy is progressive pallor of the disc. This depends chiefly
upon diminution of the capillary circulation, but it is possibly
aided by increased transparency of the nerve tissue. When the
atrophy is advanced (Plate XXXII., Fig. 73), the diagnosis is easy.
The disc margin is hard and sharp, the surface is white, tinged
with grey or blue, slightly mottled from the openings of the lamina
cribrosa showing through, and is often slightly concave. In rare
cases the disc has a greenish hue. In an early stage it is often
difficult to decide whether a slight degree of pallor is really
pathological, owing to wide differences in colour that normal eyes
present. Since the nerve fibres form a thinner layer on the outer
than on the inner side, pallor confined to the outer half of the disc
must not be diagnosed too hastily as pathological. Pallor of the
inner half is a safer guide, although even there we may be misled
by a congenital condition. In cases of doubt the disc should
always be examined by a feeble illumination. Sometimes a disc,
which under a strong light appears quite white, will then be seen
to have a distinct rose-tint.

The diagnosis will be materially assisted by taking into
consideration other points besides the ophthalmoscopic appear-

HEREDITARY OPTIC ATROPHY.

153

ance, such as the visual acuity and the field of vision.
Physiological pallor is usually equally marked in both eyes ;
it is seldom, on the other hand, that early atrophic changes
are equally advanced in the two eyes. If different degrees of
pallor on the two sides coincide with a difference in vision, there
can be no room for doubt. If the diagnosis cannot be made at the
first examination, the subsequent progress of the case will
usually reveal its nature.

The larger vessels on the disc as a rule retain their normal size,
even when simple atrophy is fully developed, although they
are sometimes slightly diminished in cases of old standing ; in
post-neuritic atrophy, on the other hand, the vessels are commonly
reduced in size. The smaller vessels, however, disappear in all
forms of advanced atrophy.

Hereditary Optic Atrophy.

This is an occasional cause of partial blindness in young
adults. It attacks several members of a family at the age of
puberty, and a history can often be obtained that others of
a previous generation have been similarly affected. The disease
shows a decided preference for males, although the females are
sometimes affected. Like other hereditary affections, it may be
transmitted through unaffected females to their offspring.

The failure of vision is more rapid in its onset than in other
forms of atrophy. The patient notices a fogginess before his
eyes, which increases in intensity, so that in the course of a few
weeks vision may be reduced to counting fingers. There succeeds
a more gradual deterioration, which usually progresses for some
months, and then ceases before total blindness is reached. In
the early stage a central scotoma is usually present, without any
general limitation of the visual fields. There may be considerable
failure of vision before any change is visible with the ophthalmoscope.
Then progressive pallor of the disc makes its appearance. This
20

154

OPTIC ATROPHY.

may be preceded by slight haziness of the disc margin, and
hyperoemia, and, in exceptional cases, by typical papillitis.

Nothing is definitely known as to the cause of the affection.
The fact that males alone are affected, and that the onset of the
symptoms coincides with the maturing of the sexual functions,
may perhaps indicate that the latter stand in some causal relation
to the disease. A history of sexual excesses can indeed sometimes
be obtained. It is probable, however, that while any marked
disturbance in the balance of the nervous system may determine
the onset of the atrophy in cases where the hereditary pre-
disposition exists, similar causes would be inoperative in a healthy
individual.

Hereditary optic atrophy was first described by Leber,1 and,
more recently, Habershon2 has given an admirable resume of all
that is known of the disease.

The history of a family in which blindness appeared in six
generations has been published by G. M. Gould.3 The main
facts are as follows : —

The males alone were affected, but the unaffected females transmitted the tendency to
their male offspring.

A feature in the family history was the high infant mortality. For example, in the
third generation there were two families descended from female members. The one
consisted of 7 males, and 1 female (who transmitted the tendency). Of the males 4
died before the age of a year, the remaining 3 developed optic atrophy at the ages of
23, 28, and 33 respectively. The other family comprised 4 males; 1 died in infancy,
the others developed atrophy at the ages of 34, 28, and 23 respectively.

This infant mortality is also noticeable in the family of a case
which was under the writer s care. I am indebted to Mr. Menteith
Ogilvie 4 for the details of the family history. In neither instance
could the infantile deaths or the miscarriages be attributed to
inherited syphilis.

1 Archiv. f. Oplith., Leipzig, bd. xvii., 1871, p. 249.

2 Trans. Oplith. Soc., vol. viii., 1888, p. 190.

3 “Ann. Ophth. Otol.” 1893.

4 Read before the Ophthalmological Society, January 30, 1896.

SECONDARY ATROPHY.

155

The patient (Allen J.) developed optic atrophy at the age of 22. His failure of vision
was accompanied by severe headache, and preceded any pallor of the discs by some months.
Eventually both discs became atrophied.

The patient’s mother had 16 pregnancies. Two resulted in miscarriages at 4 months.
Of the 14 children born alive, 8 died before the age of 16 months. Of the remaining 6,
3 were females. The 3 males became affected with optic atrophy at the ages of 15, 22, and
25 respectively.

Another peculiarity which could have no connection with the atrophy, and was common
to all the members of the family who were examined, was unusual tortuosity of the retinal
vessels. These are shown in Fig. 14, p. 51.

Secondary Atrophy.

Degenerative changes, secondary to a similar condition of the
retina, may take place in the optic disc. Atrophy of the tissue of
the retina occurs, as we have seen, in retinitis pigmentosa, and in
advanced choroiditis. It also follows embolism of the central
artery, but these cases are not included in this section.

The atrophy which is secondary to retinal degeneration,
produces an appearance which differs both from simple and from
post-neuritic atrophy. The disc is not white, but yellowish. It
is generally described as waxy, but the colour is rather that of
dirty parchment. Moreover, its surface has a flat uniform appear-
ance, and not unfrequently it is surrounded by a narrow halo of
choroidal atrophy. The vessels are always diminished in size.

The condition is difficult to depict, but it is shown to some
extent in Plate XXVIII., Fig. 62, Plate XLII., Fig. 94, Plate
XLIII., Fig. 96, Plate XLIV., Fig. 97, and Plate XLV., Fig. 98.
Probably the appearance is due to the nerve tissue becoming
atrophied without there being at the same time any great
diminution of its capillary circulation.

Gowers 1 is of opinion that waxy atrophy occurring in a young
subject, and not associated with retinitis pigmentosa, is strong
evidence of congenital syphilis.

1 “ Medical Ophthalmoscopy.1

156

OPTIC ATROPHY.

Simple Glaucoma.

Non -inflammatory, or, as it is called, simple glaucoma,
produces, in addition to the characteristic cupping of the disc, a
considerable degree of atrophy. The ophthalmoscopic appear-
ance met with in that disease may, therefore, be considered in
this place.

It must, however, be remembered that glaucoma is not primarily
an affection of the optic disc. The essential feature of the disease
is a disturbance of the balance between secretion and excretion of

Fig. 40. — Glaucomatous cup.

the intraocular fluid. The increase in the intraocular pressure
thus caused, if of sudden onset, and of considerable degree, so
impedes the circulation, that the media become turbid, and
inflammatory or congestive conditions supervene — acute, subacute,
or inflammatory glaucoma. The disease may then drift into the
chronic stage, but until this occurs the appearances of the disc,
which are typical of glaucoma, are not seen.

When, on the other hand, the increase of pressure is slight, but
long continued, the media remain clear, no congestive or inflam-

SIMPLE GLAUCOMA.

157

matory symptoms are present, and we get the characteristic
cupping of the disc — simple, or chronic glaucoma.

It would be beyond the scope of this work to discuss the causes
of simple glaucoma, and we may pass at once to the consideration
of its ophthalmoscopic appearances. These are depicted in Plate
XLVII., Figs. 105, 106, and 107. The most conspicuous change
is a pushing back, as it were, of the whole disc surface, while the
atrophy of the nerve tissue causes the edge of the disc to be seen
as a hard line, and the lamina cribrosa to become visible.

The cupping is shown in the illustrations by the abrupt curves
made by the vessels at the margin of the disc. With the
ophthalmoscope it is also shown by the parallactic movement of
the floor of the cup when the ophthalmoscope is moved in the
vertical plane, and by the fact that a concave lens is required to
focus the floor. The strength of the lens required also gives the
depth of the cup, each dioptre of refraction corresponding to 0 3 of
a millimetre of depth. It will be noted in all the illustrations
that the cupping involves the whole disc. This is a characteristic
feature of the fully-formed glaucoma cup, and affords a contrast to
the physiological cup, which never involves the whole disc.

The cupping is produced by the long continued action of a
pressure, which may not be very greatly above the normal. The
opening for the optic nerve yields, because it is a weak spot in the
outer tunic, and the lamina cribrosa is pushed back, while at
the same time the nerve tissue in front of it becomes atrophied.
Since the edge of the sclerotic coincides with the smallest part of
the nerve, it often forms a sharp overhanging edge. (Fig. 40,
page 156.)

As a rule, the retinal vessels are pushed back and follow the
outline of the cup. Occasionally, however, as in Plate XLVII.,
Figs. 106 and 107, the veins, but not the arteries, are depressed.
A frequent, but not constant, accompaniment of the glaucoma
cup, is a ring, or halo, of atrophied choroid round the disc ; this is
present in all three figures.

CHAPTER X.

AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

With the ophthalmoscope we view a terminal artery and vein
under a magnifying power of about fifteen diameters, and actually
see fluid circulating within them. Similar conditions exist nowhere
else in the body. Observation of changes in the vascular system
of the retina has therefore an important bearing on general
pathology. On the one hand, abnormal conditions of the blood
may cause impediment to the circulation, or changes in the
tissues, which, although they may be widely distributed throughout
the system, can be recognised in an early stage and with precision
only in the retina. On the other hand, widespread vascular
degeneration may first manifest itself by changes in the retinal
blood vessels.

Although conditions of the vascular system in general may
often be diagnosed with the ophthalmoscope, changes in the
cerebral circulation are not registered on the fundus with that
rapidity and precision which was at one time believed, and
which might perhaps have been expected from the intimate
anatomical connection between the vessels of the brain and the
retina.

In the first place, as already pointed out, slight degrees of
anaemia or congestion of the disc are not easy of recognition,
owing to the great individual differences in the tint of the
dsic. In the second place, the intraocular tension, acting like
the air chamber of a fire engine, tends to keep the circulation
uniform, and to prevent slight differences in the blood pressure
from effecting marked changes in the retinal circulation.

Obstruction to the return of venous blood from the retina

CHANGES IN RETINAL VESSELS.

159

produces, as we shall see, marked ophthalmoscopic changes, but
total occlusion of the cavernous sinus, into which in the normal
condition that blood flows, may exist without any fundus changes,
owing to the free anastomosis between the orbital and facial
veins.

The following are among the chief ophthalmoscopic appearances
which are due, more or less directly, to changes in the retinal
circulation : — Alterations in the width of the blood column, in
the shape of the vessel, in the breadth and brilliancy of the
light-streak, or changes in the colour of the blood. The walls of
the vessels, or the perivascular sheaths, may be abnormally
visible, or even completely opaque. There may be haemorrhages
into the retina, from which may be inferred increased blood
pressure, changes in the constitution of the blood, or disease of
the vessel walls. Lastly, there may be the group of symptoms
associated with the blocking of one of the main retinal
vessels.

Some of the above conditions are due to local, others to general
or distant causes, and their value as a means of diagnosis will be
better appreciated when we have considered in more detail the
circumstances under which they occur.

Under ordinary conditions the walls of the retinal vessels cannot
be seen with the ophthalmoscope. The width of the visible blood
column is usually assumed to indicate the diameter of the invisible
vessel. In the normal condition of the vessels this is sufficiently
accurate, because the walls are extremely thin. But in some
morbid states the vessel walls are thickened, and so opaque that
they hide the blood stream wholly or in part ; under such
circumstances the width of the blood column may afford no
indication whatever as to the diameter of the vessel.

Changes in the wall may be present without loss of trans-
parency. In retinitis pigmentosa, a hyaline thickening occurs
which encroaches on the lumen of the vessel, so that the blood
stream may appear with the ophthalmoscope as a mere thread,

160 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

although the external diameter of the vessels, when measured by
the microscope may be unaltered.

In hereditary syphilis a similar condition of the retinal vessels
is met with.1 The thickening affects chiefly the inner coat ; a
deposit of hyaline transparent substance is formed which,
gradually narrowing the lumen of the vessel, may lead to its
complete obliteration. In a later stage the resemblance to
retinitis pigmentosa is still greater, owing to the retina under-
going extensive fibroid degeneration, and its superficial layers
becoming pigmented.

In chronic Bright's disease, an analogous vascular change
is found,2 but here the thickening occurs chiefly in the outer
coat, so that the lumen of the vessel is not encroached upon. It
is said that this condition of the vessels is commonly found with
the microscope in Bright's disease, even when no ophthalmoscopic
signs have been present during life. A similar condition occurs in
the capillaries, so that they stand rigidly open on section. The
absence of any marked ophthalmoscopic evidence of vascular
change is due to the fact that the deposited material, being
transparent, is invisible, and, as the lumen of the vessel is not
encroached upon, the width of the blood column is unaltered.

Careful examination, however, will often reveal the presence of
this hyaline thickening, at the point where one vessel crosses another
(Plate XXXVI., Fig. 80, and Plate XXXVII., Fig. 84). It will
be seen that the more superficial vessel appears to pass through,
but not to fill, a gap in the deeper vessel. In fact, the appearance
is as though the vein were entirely broken through, an illusion
that is rendered the more complete by the vessel at each side
appearing darker at the point where it stops short. The
apparent gap is, no doubt, filled by the thickened artery, which,
being transparent, is invisible. The thickening of the artery,

1 Holmes Spicer, Trans. Ophth. Soc., vol. xii., p. 116; Brailey & Edmunds, Ophth. Hasp. Rep.,
London, vol. x.

2 Brailey & Edmunds, Trans. Ophth. Soc., vol. i., p. 44.

HYALINE THICKENING .

161

moreover, pushes the veins more deeply into the retina, and the
bending thus produced causes the dark colour, owing to the vessel
being seen at this point more or less “ end-011 ” (Fig. 41).

The only difficulty in accepting this explanation is, that it
would appear at first sight that the vein should be visible through
the transparent wall of the artery, but
the greater depth of the vein, and
the highly refracting nature of the
hyaline substance, probably prevent
this. It has been suggested that
the thickened artery actually impedes
the venous current at the point of
crossing ; this seems highly improb-
able, as there is no distension of
the vein on the distal side, and
none of the other effects of venous
obstruction, such as haemorrhage and
oedema.

Another result of this hyaline
thickening is that the light streak
becomes broader and extends further
along the arteries.

So far we have been dealing with
thickening of the vessel wall by a transparent substance, but the
thickening may be accompanied by opacity. For example, in a late
stage of albuminuric retinitis, degenerative changes occur in the
walls of the vessels which render them completely opaque, so that
the blood column is hidden from view, and the vessel is seen as a
white riband (Plate XL., Fig. 90). It is often impossible to be
sure whether the appearance is due to change in the wall of the
vessel or in the perivascular sheath. In the latter case, however,
the band is wider, while its margins are less regular.

We have seen that perivasculitis (as it is awkwardly called)
is sometimes associated with neuritis. It may, however, occur
21

Fig. 41. — Diagram to explain ap-
parent break in a vein where crossed
by an artery.

a, Visible blood column ; h, invisible
hyaline substance. The upper figure shows
the surface of the retina. The lower repre-
sents an imaginary vertical section at the
point of crossing.

162 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

independently of that condition. Mules1 has described and de-
picted a case of advanced renal disease, in which all the retinal
arteries were converted into white bands, and he refers to other
published cases of the condition. In some instances the amount of
deposit so greatly increases the diameter of the vessels, that, as
they approach the disc, the bands of exudation merge. The disc
may then appear to be covered by an irregular membranous
opacity, from which processes stretch out along the vessels.
These extreme cases appear to be generally of syphilitic
origin.2

Apart from changes in the vascular wall, or perivascular sheath,
real alterations in the calibre of the vessels may be met with. The
distension of the veins which occurs in neuritis has been already
considered. Enormous distension also occurs in leucocythsemia
(Plate XXXIII., Fig. 74). It must be remembered that some-
times the veins are flattened out by the intraocular pressure, and
therefore appear to be dilated. In such cases, the light streak is
either broad and indistinct, or it is absent.

Real diminution in the size of the arteries occurs in advanced
atrophy of the retina, and when they are badly filled, as in partial
occlusion by an embolus.

Aneurism of the retinal arteries is so uncommon that it
may be looked upon as an ophthalmoscopic curiosity. Both the
fusiform and the sacculated variety have, however, occasionally
been seen. Story & Benson have recorded a case3 in which
both these conditions were present in the same eye. Most of
the aneurisms formed globular swellings on the vessel wall. The
case was one of retinitis, with “considerable fibrous proliferation
and perivasculitis,” and the aneurismal dilatations were probably
due to degenerative changes occurring in the vessel wall, in
consequence of the retinitis.

1 Trans. Ophth. Soc., vol. ii., p. 47.

2 Meyer, “Alterations des parois vasculaires,” Rev. gen. d’opth., Paris, 1892.

3 Trans. Ophth. Soc., vol. vi., p. Ill; ibid., vol. iii., p. 108; ibid., vol. vi., p. 336.

NEW VESSELS IN THE VITREOUS.

163

New Vessels in the Vitreous.

In rare instances new vessels are developed from the retinal
system, and project into the vitreous. These, for the most part,
come from the disc and are very fine and convoluted. After
coming forwards a certain distance into the vitreous, the majority
form loops and return to the disc. Irregular swellings sometimes
exist at the summit of the loops, many of which can be seen to
consist of closely packed spiral turns of the vessel, while in others
the shape of the swelling suggests that they are so formed,
although the separate turns of the spiral cannot be distinguished
(see Plate XL., Fig. 91). Sometimes a more open spiral, like
the tendril of a vine, is met with in a vessel running an
otherwise straight course. The new vessels may be few in
number, and apparently unconnected with each other ; they may
be arranged in a long leash of almost parallel vessels ; or they
may form a flat-looking vascular web, resembling the mesentery
of a frog, but devoid of any visible supporting tissue. It is
probable, however, that in the latter case a transparent framework
really exists, — indeed, in some instances, this has become opaque
and visible at a later stage. Although the new vessels generally
spring from the disc and form loops, they have been known to
come from the periphery of the fundus, and to end in the vitreous
in free extremities (see case by Coccius).

Comparatively few examples of this condition have been
published, it would therefore be rash to form any conclusion
as to its cause. It may, however, be noted that diabetes was
discovered in many patients, while its existence was not excluded
in several others. In my own case the urine contained albumen,
but no sugar. Syphilis was present in a large proportion of the
patients. In several instances there had been haemorrhage into
the vitreous. It is probable that some morbid condition of the
vitreous necessarily precedes the formation of the new vessels.

164 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

Appended are short abstracts of the cases which have been
recorded : —

Coccius (quoted in Zander, “On the Ophthalmoscope”). — Punctiform opacities through-
out vitreous. Retinal veins remarkably tortuous. Numerous vessels coming forward into
vitreous. Some arising from the retinal vessels, others from the disc. Some of the vessels
ended anteriorly as white threads, others formed loops..

Jaeger (“ Hand- Atlas,” Fig. 72). — Male 27, two years before visit, temporary failure of
V. with chromotopsia after violent headache (migraine ?). Similar attack seven months
later, and again eight months after this ; a month before visit, a similar failure without
pain in head, followed by only partial recovery.

When seen, slight turbidity of vitreous chiefly near disc. Fine vessels springing from
disc, and spreading in various directions into posterior third of vitreous. Most formed
loops, having closely packed spiral turns at summit. Some of the vessels changed into
white cords, and eventually all disappeared, the fundus presenting a normal appearance
in four months.

Norris {Trans. Am. Ophth. Soc., 1879, p. 547). — Female. No history of syphilis.
Flocculi in vitreous. New vessels coming forward into vitreous, and forming loops, the
summits of which were visible with 7 B.

Charnley and Fox {Oplith. Hosp. Rep., London, vol. x., 1881, p. 193). — Girl, 19. No
history of syphilis. Iritis both eyes, four months before visit. When seen RE. = ^^
keratitis punctata. Nearly complete posterior synechia. LE. keratitis punctata below. No
synechite. New vessels in vitreous, media too turbid for accurate observation. After
treatment with mercury, vitreous cleared. Springing from OB. a large vessel which
passed straight into vitreous, and then curving upwards. was lost near equator. A group
of small vessels springing from centre of OB. passed into vitreous, most formed loops and
returned to point of origin. An anterior extremity of loops, spiral coils. Five months
later vessels had entirely disappeared, and Y. normal.

Charnley and Fox ( loc . cit.).- — Girl, aged 14. RE. had been operated on for internal
strabismus. V. ec. in each eye. Ophthalmoscopic appearances not noted till three
months later.

RE. margins of OB. hazy. Vessels enlarged and slightly tortuous. A figure shows
a single fine vessel spring from OB. below its centre, one branch of this soon terminates in
a fine loop, the other makes five spiral turns, and later on divides into three branches, each
of which terminates in a loop. A similar vessel emerging from above the disc makes six
spiral turns, and returns to its point of exit ; a fine supporting framework of connective
tissue supported this vessel. In the YS. region were traces of old choroiditis.
After five months mercurial treatment, vitreous clearer, vessels smaller.

Charnley and Fox {loc. cit.). — Woman, 51 (Mr. Fitzgerald’s case). Seen April 1st,
1880.

RE. V. = Nj) clots in vitreous. No history of syphilis. No albumen in urine. Eight
months later, vitreous slightly hazy. Below OB. a small greyish spot of connective tissue

NEW VESSELS IN THE VITREOUS.

165

on retina, from which springs a bunch of vessels upwards and forwards into vitreous.
Some present free extremities, others form loops and return to point of origin. Spiral
twists at summit of loops. The vessels float freely in vitreous. No detachment of retina.
The vitreous subsequently became too hazy for ophthalmoscopic examination.

Hirschberg ( Gentralbl . f. prakt. Augenh., Leipzig, 1881, p. 48). — Woman, 23. There had
been choroido-retinitis with blurring of 01)., and haemorrhages in both eyes. On vitreous
clearing, the vessels were seen.

Hirschberg {Gentralbl. f prakt. Augenh., Leipzig, 1883, p. 325). — Woman, 60. Failure
of V. in both eyes, worse in LE., in which punctate retinitis. In BE. vessels spring into
vitreous from OD. in all directions, except up and in, most formed loops and returned to
point of origin, swelling at summit of some of the loops. Urine examined for excess of
urea without result. Albumen and sugar not mentioned.

Nettlesiiip {Trans. Ophth. Soc., vol. iv., 1884, p. 150). — John K., 50. Seen August 1883.
Y. failing seven months ; the LE. first. Had had choroiditis a year previously, followed by
secondary symptoms.

LE. opacities in vitreous. Extensive detachment of retina.

BE. and 16 J., a posterior synechia below. Numerous webs in vitreous. A good
many rounded htemorrhages of rather small size on fundus, chiefly at upper periphery, also
several dark ones, apparently in front of retina near YS. Two weeks later, a close meshwork
of very small tortuous vessels on the outer side of disc, and another patch of vessels on
inner side. No evidence of obliteration of any of the central vessels. Disc, pale and hazy.
The vitreous became clearer, and on October 23rd drawing (reproduced) was made.
There is a flat transparent vascular membrane attached to the outer border of OD., and
projecting straight forwards into the vitreous. Its vessels are looped and very numerous.
One larger one forming its anterior free border. The top of the membrane visible with
4 D.

December 6th. Condition unaltered, except that the haemorrhages have dispersed. Still
some fine webs in vitreous. V. 14 J., barely, January 14th, 1884. The web was bent
over to the nasal side.

February '21st. Two fresh growths of vessels have appeared in form of long narrow
leashes, one passing up and out, the other inwards, from the upper part of the disc. The
original membrane has bent over still more towards the nasal side of the disc. These
conditions are shown in a second figure.

August 21st. V. 14 J. Fundus much as last note, but a good deal of white
opacity (connective tissue ?) about the bases of some of the vascular growths.

The veil-like growth at the disc has turned, so that it is now nearly horizontal, instead
of vertical as before.

Communicated by Mr. Ernest Clarke. — A. B., 19, actress. First seen February
26th, 1887. History of syphilis. Y. BE. =A

LE. N- Yitreous very hazy from fine dust-like opacities. On the outer side of the
OD. apparently spring from the central artery two vessels which came forward into the
vitreous. Both were tortuous, the upper one being cork-screw shaped ; they formed loops,
the extremities of which moved about freely with the ocular movements. Under iodide of

166 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

potassium the vitreous cleared, and Y. improved to but the vessels remained unchanged
during the two months the patient was under observation.

Cakmalt (Trans. Am. Ophth. Sac., 1887, p. 545). — Case mentioned in which
haemorrhages into vitreous were followed by formation of vessels running from retina nearly
to lens. They formed loops twined among each other.

Theobald (Trans. Am. Ophth. Soc., 1887, p. 542). — Woman, 52. Repeated small
hemorrhages into retina near OR., which was swollen ; retinal veins distended. Later a
globular hemorrhage the size of the disc into vitreous. This disappeared, and Y. became
normal. A few weeks V. improved to normal. Then fresh hemorrhages and brownish
string-like opacities. Y. again became normal. Then a reddish, nebulous floating opacity
seen in front of OR., which seemed a few weeks later to consist of a mass of blood vessels.

Nettleship (Trans. Ophth. Soc., vol. viii., 1888, p. 159). — Charles 0., 48. Diabetes. Three
to four years. Y. began to fail about same time. No gout or syphilis. No albumen. When
seen the LE. was blind from glaucoma, secondary to iritis. RE. Over whole central region
retina cedematous and hazy ; in some parts densely cloudy. Near YS. some densely
opaque yellowish white masses of deposit. Retinal vessels considerably distended, and in
various parts a few scattered blood spots. Close to fovea two or three vessels of medium
size suddenly appear in retina, having every appearance of springing directly from choroid
into retina. The largest, followed up and out, divides into a network of minute vessels,
which project forward in the form of fine loops into vitreous, where the most prominent are
seen with 6 R. On a few are small swellings, perhaps capillary aneurisms.

Author’s Case (unpublished). — Woman, 54. First seen June, 1889. LE.,
RE. -If. The failure of vision stated to be recent. There was luemorrhage at the yellow
spot. Urine pale, 1022. Trace of albumen. No sugar. Suffers from giddiness, headache,
and oedema of feet. Patient lived at a distance, and was not seen again till November.
Then vessels seen springing from disc, and extending into vitreous (Plate XL., Fig. 91).
Later a gauze-like material became visible, accompanying the vessels, and soon afterwards
the vitreous became opaque.

Hirschberg (Centralbl. /. prald. Augcnh., Leipzig, 1889, p. 8). — Man, 47. Had syphilis
a year previously. Punctiform opacities in vitreous. A striated haemorrhage in retina.
Slight optic neuritis. Improved, but some months later V. became worse. A bluish mass
of connective tissue seen on disc, hiding exit of vessels. Extending upwards and inwards
21 dd., a vascular web, resembling framework of a fly’s wing, as seen under the microscope.

Harlan (Trans. Am. Ophth. Soc., 1889, p. 426). — Female, 50|. A year before visit an
inflammatory attack in LE., which recovered in three months.

Five months before visit, rapid or sudden failure of Y. in RE. When seen, V.
RE. yellowish white spots on US', region ; remains of old haemorrhages. Yitreous
quite transparent. Vascular web springs from disc, and projecting into vitreous at an angle
of 45°. The web appeared to consist of vessels only, no stroma being visible.

In LE. remains of haemorrhage at YS.', vitreous hazy. Vessels springing into vitreous
from OR., but fewer. Urine, trace of albumen ; no casts. One month and again four months

INTRAOCULAR HAEMORRHAGE.

167

later, fresh haemorrhages occurred. RE. without change in web. Eight months after visit
vitreous hazy ; slight keratitis punctata. Most of the vessels had disappeared ; others
reduced to dark lines. V.

J. Hutchinson, Jun. {Ophth. Hosp. Rep., London, vol. xi., p. 191). — Thos. 11., 28.
Remains of optic neuritis in both eyes. RE. 19 J., IE. 16 J. There was a
strong probability of syphilis.

RE. In front of OR., covering a considerable part of its outer half, a patch of small
new vessels, surrounded by lymph, and projecting 6 J). into vitreous.

At first it was thought that there were several small vessels. As the lymph cleared away
under antisyphilitic remedies ; a single small branch was seen to come off from the central
artery, and to coil itself up in a corkscrew manner. In the LE. the conditions were similar,
but less marked, and ultimately disappeared. A year later all lymph had disappeared, only
a beautifully coiled single vessel remaining.

The same author publishes another case in which in each eye there was a crescentic
patch of vascularised lymph placed nearly vertically over each disc. There had been optic
neuritis, and the patient had had syphilis.

Elschnig {Arch. Ophth. and Otol., N. Y., vol. xxii., p. 75). — A case of embolism of
the central artery. Partial restoration of the circulation, but the disc became atrophic. A
month after the occurrence of embolism, a loose greyish tissue was seen over supero-temporal
quadrant of disc, projecting into vitreous, carrying fine vessels and vascular networks.
Three months later a fine network of vessels covered the entire disc.

Intraocular Hemorrhage.

Among affections of the vascular system of the retina, haemor-
rhage claims an important place, from the frequency with which
it occurs either alone, or as a complication of other conditions. It
is common in all forms of retinitis, but is especially frequent in
that associated with renal disease. It is met with in a considerable
number of cases of papillitis, in which there is much swelling of
the disc. Lastly, it may occur in any condition which involves
grave alteration of the blood, as, for example, anaemia,1 scurvy,
or leucocythaemia.

The capillaries are the source of the bleeding in nearly all
cases. Even the more copious extravasations, which might be
thought to be furnished by larger vessels, are commonly preceded
by smaller haemorrhages, which are certainly of capillary origin.
In renal disease the walls of the capillaries are in a condition

1 Mackenzie, Trans. Ophth. Soc., vol. i., p. 48; ibid., vol. ii., p. 40; ibid., vol. iv., p. 132.

168 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

which predisposes to haemorrhage. In papillitis, from any cause,
the pressure on the walls is increased by the obstruction to the
circulation caused by the inflammatory exudation into the nerve
head. In the other cases enumerated above, the alterations in the
character of blood permit its more ready exudation through the
capillary walls.

The ophthalmoscopic appearance produced by a haemorrhage
will depend upon its depth in the retina. The most common
situation is the fibre layer, and the blood has then a distinctly
striated arrangement. This is seen in Plate XXXV., Fig. 79.
Also in the haemorrhages near the disc in Fig. 79. Solitary effusions
of blood into the fibre layer form what are sometimes spoken
of as flame-shaped haemorrhages. Examples may be seen in
Plate XXXVII., Fig. 84, and Plate XXXI., Fig. 68. When
several such haemorrhages lie in the same line, the appearance may
resemble a vessel, the course of which is partially concealed from
view. This is the case to some extent in Plate XXXV., Fig. 78.
But when there is at the same time much swelling of the retina
the resemblance is much closer.

When extravasation of blood takes place into the other layers
of the retina, it is seen either as a granular area formed by the
aggregation of small red dots, as some of the haemorrhages in
Plate XXXV., Fig. 78, or as an irregular patch, as in Plate
XXXVII., Fig. 83.

Extensive retinal haemorrhage is occasionally met with in old
people (Plate XXXV., Fig. 79). The condition, which is usually
attributed to degenerative changes in the walls of the vessels,
has sometimes been called retinitis apoplectica, from a supposed
analogy between it and cerebral apoplexy. The retinal vessels are,
however, far below the size of those which are known to undergo
atheromatous changes, and the retinal affection does not seem to
indicate any special liability to cerebral haemorrhage. The con-
dition makes its appearance suddenly, and the haemorrhages take
place in all parts of the retina almost simultaneously. Although

INTRAOCULAR HAEMORRHAGE.

169

the disc is little, if at all, swollen, the veins are often distended
and tortuous. It is probable that in most of these cases the
cause of the ophthalmoscopic conditions is thrombosis of the
central vein. This subject will be referred to later on.

Retinal haemorrhage occurs not unfrequently in association

with glaucoma, but the nature of the connection between

the two conditions is not understood. In these circumstances

the extravasations are numerous and of small size. Occasionallv

the blood flows into the glaucomatous cup, as in a case
recorded by Hartridge.1 The papilla then presents a blood
red surface ; the vessels appearing to emerge from behind a disc
of red.

Extravasation may take place beneath the hyaloid membrane.
The blood then spreads equally in all directions, and therefore
forms a thin layer of nearly uniform colour, with a circular
contour. Haemorrhages of this kind are most frequently seen
in the region of the macula. When they occur in other
situations, they are usually less regular in outline.

In sub-hyaloid haemorrhage in the macular region, the blood,
from the action of gravity, tends to sink to the lower part of
the affected area. Hence we may get bagging of the blood
below, and its complete disappearance above. The line marking
the upper limit of the blood may, in this event, be perfectly
straight, so that the patch has now the shape of a D with
its convexity directed downwards. These points are seen in
Plate XXXIX., Fig. 88. The greater amount of blood near the
lower margin is shown by the darker colour ; the thinness of
the layer elsewhere by the fovea centralis being visible
through it, and by the fact that the patient can see objects
although they appear to be covered by a red veil. The
outline is usually more regular than in this instance. When
first seen the haemorrhage had the form depicted, and there was
nothing to indicate that it had ever extended further. In a few

1 Trans. Ophth. Soc., vol. xi., Plate IV.

170 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

days, however, a remarkable change occurred in the retina
immediately above, apparently indicating the extent to which
the hyaloid had been detached ; this consisted in a change of
colour to a slate-grey. At the same time this area, and that
still occupied by blood, became sprinkled with minute dots of a
crystalline appearance. Meanwhile the layer of blood had become
somewhat thinner, so that retinal vessels previously hidden had
again become visible.

Masselon 1 2 has recorded an interesting case, in which the
straight boundary of a semicircular haemorrhage varied with
the position of the patient’s head so that its direction was
always horizontal. As the blood thus shifted its position retinal
vessels previously concealed again became visible. Evidently,
therefore, the straight boundary of the extravasation was due
to the action of gravity upon fluid blood lying free in a cavity.
Such an explanation, however, would not apply to the case
published by Silcock in which the straight border was below,
and oblique in direction.

The prognosis in these circular haemorrhages, is more favourable
than in the other forms, owing to the thinness of the layer
of blood, and to the fact that the tissue of the retina is not
implicated.

It has been suggested that these haemorrhages are choroidal
and not sub - hyaloid. The evidence, however, in favour of
their being sub-hyaloid is very strong. The sharpness of their
outline is not consistent with extravasation into a tissue like the
choroid, and in many instances the patient has seen external
objects as through a red veil, showing that the layer of blood
is at any rate in front of the layer of rods and cones. The
colour of the extravasation being nearly that of the vessels,
it is not easy to be certain of the relation of the latter
to the haemorrhage ; but in a case observed by Stanford

1 “ La clinique Ophtalmologique,” p. 19, 1895.

2 Trans. Ojphth. Soc., vol. vii., p. 176.

INTRAOCULAR HAEMORRHAGE.

171

Morton,1 this doubt was set at rest by the area of extravasation 2
becoming white after some months, and it could then be distinctly
seen to lie in front of the vessels.

To return to retinal haemorrhages in general : — sometimes
patches of extra vasated blood present no appreciable change even
after some months, but they usually become darker. When the
layer of blood is thin, as in the cases of sub-hyaloid extravasa-
tion just described, complete absorption may take place. In other
instances yellowish white or white patches are left, due to fatty
degeneration of the disturbed retinal tissue, such as are to be seen
in Plate XXXV., Figs. 78 and 79. Sometimes minute crystalline
bodies can be seen on the surface of these. Eventually these
patches may entirely disappear and there may be nothing to
mark the site of the haemorrhage. It is, however, very common
for pigment spots to persist ; these are probably not due to blood
pigment, but to disturbance of the pigmentary layer of the retina
which causes it to proliferate.

Exceptionally, the layer of blood is so thick, or its colour
so dark that no light is reflected through it from the choroid. It
would seem that such transmitted light is necessary to give the
red colour. In its absence we get a dark slate colour, even
darker than that depicted in Plate XXXIX., Fig. 89. If the
area occupied by this colour is large, the loss of light may render
ophthalmoscopic examination difficult or impossible. In such
cases a better view can often be obtained by the indirect method,
because a larger portion of the fundus is then seen and sufficient
light is obtained from the part not occupied by the extravasation.
In some of these cases of slate coloured extravasation the blood
is probably beneath the retina. Under such circumstances the
retinal vessels may be visible over the grey area.

Hsemorrhage from retinal vessels is sometimes so copious that

1 Trans. Ophth. Soc., vol. ix., p. 145, with chromolithograph.

2 Good examples of 0-shaped extravasations are to he seen in the illustrations which accompany
the following papers : — Trans. Oplitli. Soc., vol. iv., p. 148; ibid., vol. vi., p. 335; ibid., vol. viii.,

172 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

it bursts through into the vitreous, which may then be too
opaque for the source of the bleeding to be discovered. It is
probable that the majority of vitreous haemorrhages are derived
from the ciliary processes. When, however, a copious extravasation
into the vitreous has been preceded by smaller haemorrhages
into the substance of the retina, it is a fair inference that both
come from the retinal vessels.

Haemorrhages into the vitreous may occur at all periods of
life. They are especially frequent in women at the climacteric.
They also occur in young men, but these latter cases present such
definite characteristics that they constitute a distinct clinical
group calling for separate consideration.

Recurrent Intraocular Haemorrhage in Young Men.

Young men, not suffering from any obvious impairment of
health, and following their usual occupations, are occasionally
attacked by sudden and profuse intraocular haemorrhage, which
leads to serious impairment of sight. Considering the amount
of blood poured out, vision often recovers with surprising
rapidity, but the liability to relapse renders the prognosis most
grave.

Attention was first called to these cases by Eales1 in 1880.
Four instances have since been recorded by Hutchinson,2 two by
Abadie,3 and others from time to time by various authors.

The extravasation may take place into the substance of the
retina, but usually it breaks through into the vitreous. It may
be so copious that satisfactory ophthalmoscopic examination is
rendered impossible. There may be only a faint fundus reflex,
and the vitreous may be seen to contain a gauzy film of
blood.

1 Birmingham Med. Rev., July 1880, and Ophth. Rev., London, 1882.

2 Trans. Ophtli. Soc., vol. i., p. 26.

3 Ann. d’ocul., Bruxelles, 1886, p. 36.

RECURRENT INTRAOCULAR HAEMORRHAGE.

173

Smaller extravasations in the retina sometimes precede the
large haemorrhage into the vitreous. They may be accompanied
by retinitis, but in many instances an extensive bleeding into the
vitreous has occurred without any premonitory symptoms.

Numerous causes have been assigned for these haemorrhages,
but it cannot be said that their pathology is thoroughly
understood. Constipation has existed in many of the patients,
and in some there has been a history of repeated epistaxis, but
apart from this, none of the published cases appear to have
shown any indication of the haemorrhagic diathesis. A gouty
history may now and then be obtained, and Mr. Hutchinson is
inclined to attach considerable importance to this as an etiological
factor.

The following case (which was under the care of the writer, and
of Dr. Nelson of Belfast), may be cited as an example : —

Repeated haemorrhages into vitreous, resulting in blindness.

Mr. G. P., 27. A tall muscular man, of slightly anaemic aspect, was first seen by
the writer on September 12th, 1889. He was very deaf from nerve disease, for which he
had been treated in October 1888 with mercury, pushed to salivation. About this time he
noticed failure of vision, and saw Mr. Nelson, who kindly furnished me with the following
note as to his condition : —

Some haziness of retinae near discs. In LE. some lnemorrhages and whitish exudation.
Two days later a fine gauzy film in each vitreous. V. §£ each eye. During the next few
weeks a whitish exudation occurred along the vessels near the disc, and several haemorrhages
occurred. By February both eyes had cleared considerably.

The patient believes that after this his vision recovered completely. At any rate,
until five days before his visit to the writer, he could read small print without difficulty.
Then a rapid deterioration occurred, and when seen V. RE. some letters picked out
slowly ; LE. N

In RE. a large floating dark mass in vitreous, and the upper part of the retina was
studded with small haemorrhages. LE. floating film in vitreous. No swelling of disc.
Visual field normal in each eye.

There was no history of constipation or epistaxis, and no evidence of a haemorrhagic
diathesis. Mr. Hutchinson was of opinion that the patient had had syphilis. The writer
and some others who examined the patient with especial reference to this point, failed
to obtain any evidence of this. There was a strong history of gout on his mother’s side,
but the patient himself had not suffered.

The blood was examined by Dr. Cavafy, who found the corpuscles normal in number,
the red a little pale, some oval or flask-shaped. A recognisable quantity of hsematoblasts
and microcytes. Heart, lungs, and urine normal.

174 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

The patient was treated with purgatives, iron, and then subcutaneous injections of
pilocarpine. Vision improved to RE. £ and LE. but it varied much owing to the
movements of the opacities.

In February, 1890, he had influenza, and on recovering suffered from large haemorrhage
into the left vitreous. This was absorbed, but a relapse occurred and reduced vision to
bare p.l. In April there was no p.l. in the LE. and no fundus reflex. Vision RE. = £, but
during the next four months three attacks of haemorrhage occurred, the last reducing
vision to bare p.l.

Arterial Embolism and Thrombosis.

We have seen that the retinal circulation is terminal, or
entirely dependent upon the artery and the vein which pass
along the centre of the optic nerve. Hence, if either of these
vessels becomes occluded, marked symptoms rapidly make their
appearance.

Occlusion of the arteria centralis retince. — The arteria centralis
may become occluded either by a clot carried into it from a
distance — embolism ; or by coagulation taking place in situ —
thrombosis. The ophthalmoscopic signs are identical and due to
the sudden arrest of the circulation. The disc immediately
becomes a dead white colour. The arteries may be only slightly
smaller than normal, reduced to mere threads, or even altogether
invisible. The light-streak is absent from them, and they may
so closely resemble the veins in colour that a distinction cannot
be made with certainty. The veins, as a rule, are either normal,
or slightly reduced in size ; occasionally they taper towards the
disc. Pressure on the globe fails to produce pulsation in
either set of vessels. Sometimes the blood stream, both in
arteries and veins, but more frequently in the former, is divided
into segments, like the column of mercury in a broken
thermometer, portions of blood alternating with what look like
spaces. Doubtless some of these gaps are portions of the vessel
that are really empty and collapsed, while others in which the
diameter of the vessel is maintained are probably filled with
liquor sanguinis.

EMBOLISM OF CENTRAL ARTERY.

175

A similar interruption of the blood column has been seen in the
retinal vessels of animals recently killed.1 The colourless spaces
contained no red corpuscles, but were filled with blood plasma and
white corpuscles. The red corpuscles were heaped together in the
coloured portions of the vessels.

Within an hour or so after the arrest of the circulation by a clot,
marked changes occur in the retina. Its tissue becomes opaque,
and of a uniform soft-looking white colour. This is most marked
in the neighbourhood of the disc, but often reaches to the periphery
of the fundus.

The macula itself escapes, and is seen as a cherry-red spot
amid the surrounding white. This spot looks like a haemorrhage,
but most authorities are now agreed that it is really the natural
colour of the fovea accentuated by contrast with the white fundus.
Small haemorrhages into the retina do, however, now and then
occur in cases of embolism. This appearance of the macula is seen
in Plate XLI., Figs. 92 and 93, but it is less conspicuous than
is sometimes the case. The absence of visible change at the
macula is not accompanied by any retention of its functional
activity.

The appearance of the retina closely resembles that presented
by oedema (Plate XXV., Fig. 58) ; it is, however, probably
due rather to what might be called post-mortem changes in its
tissue than to true oedema.

Later the collapsed arteries contract, and the small amount
of blood which they contain being pressed out, they become
nearly or quite invisible. The contraction is more marked near
the disc, the vessels at the periphery of the fundus may even
retain their normal calibre, while at the disc they taper down
to mere threads. As already mentioned, the veins also are often
smaller at the disc ; probably the appearance in both cases is
caused by the intraocular pressure forcing blood out of the eye
along the vessels in which the resistance is diminished.

1 Friedenwald, Ophth. Rev., London, vol. xii., p. 161.

176 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

At a still later stage the vessels may again become visible,
or even abnormally conspicuous, in consequence of degenerative
changes taking place in their walls, converting them into white
bands (Plate XLI., Fig. 92). Meanwhile the disc passes into a
condition of complete atrophy, and the degeneration may spread
up the nerve as high as the chiasma.

Even in the latest stage it is not uncommon for the arteries
to carry a thin stream of blood. In such cases either the embolus
has shrunk and so allowed some blood to trickle past, or a
collateral circulation has been established.

A shrinking of the clot has been found in several cases where
a post-mortem has been obtained. In some of these, although the
symptoms during life had indicated that the vessel was completely
occluded, the clot was found after death adhering to one side of
the vessel, covered by endothelium, and only slightly encroaching
on the lumen of the vessel ; in two cases in which the symptoms
were typical, examination made at eighteen months1 and three
years 2 respectively, revealed nothing abnormal in the arteries.

Collateral circulation, on the other hand, has never been
proved post-mortem, although it has occasionally been suggested
by the clinical evidence. Assuming that it can occur, the most
obvious collateral channels are the vessels in the sclerotic, derived
from the short ciliary arteries which form the circle of Haller.
It has also been suggested that blood may possibly enter the
arteries at a peripheral part of the retina, although no anatomical
anastomosis exists there. The grounds for this latter assumption
are that the arteries in embolism are often larger towards the
periphery ; that recovery of circulation has occurred where the
clot lay anterior to the lamina ; and that in a case of Hirschberg’s
(which will be referred to later) the blood was seen to move in the
artery from the periphery towards the disc. Not one of these
reasons is, however, of much weight.

1 Hirschberg, Centralbl. f. prakt. Augenli., Leipzig, 1884, p. 7.

2 Popp, Inaug., Diss. 1875 (extract in Ophth. Hosp. Rep., London, vol. viii., p. 616).

INTRAOCULAR HEMORRHAGE.

169

Retinal haemorrhage occurs not unfrequently in association

with glaucoma, but the nature of the connection between

the two conditions is not understood. In these circumstances

the extravasations are numerous and of small size. Occasionallv

«/

the blood flows into the glaucomatous cup, as in a case
recorded by Hartridge.1 The papilla then presents a blood
red surface ; the vessels appearing to emerge from behind a disc
of red.

1 Trans. Oplith. Soc., vol. xi., Plate IV.

170 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

published by Silcock in which the straight border was below,
and oblique in direction.

The prognosis in these circular haemorrhages, is more favourable
than in the other forms, owing to the thinness of the layer
of blood, and to the fact that the tissue of the retina is not
implicated.

It has been suggested that these haemorrhages are choroidal
and not sub - hyaloid. The evidence, however, in favour of

their being sub-hyaloid is very strong. The sharpness of their
outline is not consistent with extravasation into a tissue like the
choroid, and in many instances the patient has seen external
objects as through a red veil, showing that the layer of blood
is at any rate in front of the layer of rods and cones. The
colour of the extravasation being nearly that of the vessels,
it is not easy to be certain of the relation of the latter

to the haemorrhage ; but in a case observed by Stanford

1 “ La clinique Ophtalmologique,” p. 19, 1895.

2 Trans. Ojphth. Soc., vol. vii., p. 176.

INTRAOCULAR HEMORRHAGE.

171

Morton,1 this doubt was set at rest by the area of extravasation 2
becoming white after some months, and it could then be distinctly
seen to lie in front of the vessels.

To return to retinal haemorrhages in general : — sometimes
patches of extravasated blood present no appreciable change even
after some months, but they usually become darker. When the
layer of blood is thin, as in the cases of sub-hyaloid extravasa-
tion just described, complete absorption may take place. In other
instances yellowish white or white patches are left, due to fatty
degeneration of the disturbed retinal tissue, such as are to be seen
in Plate XXXV., Figs. 78 and 79. Sometimes minute crystalline
bodies can be seen on the surface of these. Eventually these
patches may entirely disappear and there may be nothing to
mark the site of the haemorrhage. It is, however, very common
for pigment spots to persist ; these are probably not due to blood
pigment, but to disturbance of the pigmentary layer of the retina
which causes it to proliferate.

Haemorrhage from retinal vessels is sometimes so copious that

1 Trans. Ophth. Soc., vol. ix., p. 145, with chromolithograph.

2 Good examples of 0-shaped extravasations are to he seen in the illustrations which accompany
the following papers : — Trans. Ophth. Soc., vol. iv., p. 148; ibid., vol. vi., p. 335; ibid., vol. viii.,

172 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

Recurrent Intraocular Haemorrhage in Young Men.

Attention was first called to these cases by Eales1 in 1880.
Four instances have since been recorded by Hutchinson,2 two by
Abadie,3 and others from time to time by various authors.

1 Birmingham Med. Rev., July 1880, and Ophth. Rev., London, 1882.

2 Trans. Ophth. Soc., vol. i., p. 26.

3 Ann. d’ocul., Bruxelles, 1886, p. 36.

RECURRENT INTRAOCULAR HAEMORRHAGE.

173

The following case (which was under the care of the writer, and
of Dr. Nelson of Belfast), may be cited as an example : —

Repeated haemorrhages into vitreous, resulting in blindness.

Mr. G. P., 27. A tall muscular man, of slightly ana?mic aspect, was first seen by
the writer on September 12th, 1889. He was very deaf from nerve disease, for which he
had been treated in October 1888 with mercury, pushed to salivation. About this time he
noticed failure of vision, and saw Mr. Nelson, who kindly furnished me with the following
note as to his condition : —

Some haziness of retime near discs. In LE. some hemorrhages and whitish exudation.
Two days later a fine gauzy film in each vitreous. V. -§£ each eye. During the next few
weeks a whitish exudation occurred along the vessels near the disc, and several hemorrhages
occurred. By February both eyes had cleared considerably.

The patient believes that after this his vision recovered completely. At ary rate,
until five days before his visit to the writer, he could read small print without difficulty.
Then a rapid deterioration occurred, and when seen Y. RE. § some letters picked out
slowly ; LE.

174 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

The patient was treated with purgatives, iron, and then subcutaneous injections of
pilocarpine. Vision improved to RE. £ and LE. T*L, but it varied much owing to the
movements of the opacities.

In February, 1890, he had influenza, and on recovering suffered from large haemorrhage
into the left vitreous. This was absorbed, but a relapse occurred and reduced vision to
bare p.l. In April there was no p.l. in the LE. and no fundus reflex. Vision RE.=%, but
during the next four months three attacks of haemorrhage occurred, the last reducing
vision to bar e p.l.

Arterial Embolism and Thrombosis.

Occlusion of the arteria centralis retinae. — The arteria centralis
may become occluded either by a clot carried into it from a
distance — embolism ; or by coagulation taking place in situ —
thrombosis. The ophthalmoscopic signs are identical and due to
the sudden arrest of the circulation. The disc immediately
becomes a dead white colour. The arteries may be only slightly
smaller than normal, reduced to mere threads, or even altogether
invisible. The light-streak is absent from them, and they may
so closely resemble the veins in colour that a distinction cannot
be made with certainty. The veins, as a rule, are either normal,
or slightly reduced in size ; occasionally they taper towards the
disc. Pressure on the globe fails to produce pulsation in
either set of vessels. Sometimes the blood stream, both in
arteries and veins, but more frequently in the former, is divided
into segments, like the column of mercury in a broken
thermometer, portions of blood alternating with what look like
spaces. Doubtless some of these gaps are portions of the vessel
that are really empty and collapsed, while others in which the
diameter of the vessel is maintained are probably filled with
liquor sanguinis.

EMBOLISM OF CENTRAL ARTERY.

175

1 Friedenwald, Ophtli. Rev., London, vol. xii., p. 161.

176 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

Collateral circulation, on the other hand, has never been
proved post-mortem , although it has occasionally been suggested
by the clinical evidence. Assuming that it can occur, the most
obvious collateral channels are the vessels in the sclerotic, derived
from the short ciliary arteries which form the circle of Haller.
It has also been suggested that blood may possibly enter the
arteries at a peripheral part of the retina, although no anatomical
anastomosis exists there. The grounds for this latter assumption
are that the arteries in embolism are often larger towards the
periphery ; that recovery of circulation has occurred where the
clot lay anterior to the lamina ; and that in a case of Hirschberg’s
(which will be referred to later) the blood was seen to move in the
artery from the periphery towards the disc. Not one of these
reasons is, however, of much weight.

1 Hirschberg, Centralbl. f. prakt. Augenh., Leipzig, 1884, p. 7.

2 Popp, Inaug., Diss. 1875 (extract in Ophth. Hosp. Rep., London, vol. viii., p. 616).

RE-ESTABLISHMENT OF CIRCULATION.

185

vessels very small, the veins on and near the disc pulsating, V. = p.l. Next day (6 th), a
pulsating centripetal movement in veins.

8 th day— Blood column in inferior nasal artery interrupted by a small white cylinder.
Spontaneous venous pulsation, slight arterial pulsation on pressure. Eetinal opacity less
marked.

12 th day. — Short red blood-cylinders passing into superior nasal artery and its two
terminal branches. In the course of an hour this movement ceased, the blood from one of the
branches passed in the reverse direction, partly into the main trunk and partly into the other
branch. Later the normal direction was resumed. This process was frequently repeated.

13 th day. — Circulation sometimes suddenly stops and then begins again. Eventually
the disc became atrophic. New vessels projected from it into the vitreous.

Hirschberg explains the reversed arterial current on the
hypothesis of an anastomosis between the arterial systems of the
retina and choroid in the ciliary region. There is, however, no
anatomical evidence of this, and the phenomenon may be accounted
for in other ways. For example, if there were a valve-like clot
situated at a bifurcation of an artery which allowed blood to pass only
into one division, the current might, by exercising a suction action,
draw blood from the occluded vessel. Again, a reversed current may
result as suggested by Elschnig, simply from the lowered pressure
in the collapsed vessel. As soon as an artery becomes plugged,
the blood pressure in it and all its branches on the distal side of
the obstruction sinks to that of the intraocular pressure, the blood
pressure in the veins will for a short time remain almost at its
normal height ; hence there will be a tendency for the blood
in the capillaries to flow back into the arteries until the pressure in
the arteries and veins is equalised. If only the upper or the lower
artery were plugged, the other remaining patent, an anastomosis
between the corresponding venous systems, might keep the blood
pressure in the vein constantly higher than in the affected artery.

The following cases seem to point to a plugging either
incomplete at first or becoming so later on : —

Embolism — Alternate filling and collapsing of artery on disc occurring rhythmically —
autopsy (Hirschberg, Centralbl. f. prakt. Augenh., Leipzig, 1884, p. 2). — The patient,
a man aged 45, was seen four hours after sudden loss of vision of RE. No p.l. Usual signs
of embolism present. Next day the blood column in the veins was in segments which
travelled slowly towards the disc.

186 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

2nd day. — This movement was less, sometimes stopping.

3rd day. — More oedema, primary branches of arteries well filled, those of second
magnitude small, but not thread-like, veins dark, not small, no visible movement.

Ath day. — The following curious rhythmical movement noted: — On the disc the
upper and lower divisions of the central artery were in line, thus forming what was
practically a single vertical vessel, hut the main trunk of the central artery was
not itself visible. On the previous day this vertical vessel had been well filled,
now it was empty forming a narrow white band. Above and below it bifurcated, the
branches being of fair size. A little below the centre of the vertical vessel, there appeared a
small cylinder of blood which gradually elongated till it reached the bifurcation above and
below, the whole vessel thus being filled. After a short time it would again empty, and
the phenomenon would be repeated. This only occurred a few times, and the vessel then
remained full. The oedema gradually subsided, but the disc remained white, and the
arteries and veins became smaller towards the disc than at the periphery. The patient
died six months after the occurrence of the embolism. The plugged artery was not
discovered at the autopsy, but the vessel between its origin and its point of entry into the
nerve seems not to have been fully examined.

The next case in which the artery was only partially blocked
is important since it was completed by an autopsy.

Incomplete embolism — Autopsy three months later (Schnabel and Sachs, Arch. Ophth.
and Otol., N.Y., vol. xiv., p. 263). — Paul G., 33. Endocarditis two years previously. Seen
fifteen hours after sudden failure of LE. Disc, blue-grey, its margin blurred. Arteries and
veins on OD. reduced to threads, and not to be distinguished from each other. At the periphery
they were fuller, and were distinguishable. Twenty-four hours after the loss of vision the
arteries of normal size. Veins fuller than before, hut smaller than the arteries. They
narrowed towards the disc. Slow intermittent movement of blood column in the veins
towards the disc. A sudden blindness of the RE. occurred one day, and lasted five minutes.
The patient died three months after the occurrence of the embolism.

Autopsy 48 hours after death. Extensive cardiac lesions. Situated at the level of the
lamina cribrosa, an embolus whose length was twice the diameter of the vessel. It was
partly granular and partly hyaline. One part was attached to the vessel wall, the
remainder projected into the lumen of the vessel, two-thirds of which it occluded.
Endothelium had grown over the clot, shielding it from direct contact with the blood.
Behind the embolus the vessel was of normal calibre. There was no dilatation of the
vessels entering the nerve from the circle of Haller. Extensive atrophic changes in the
nerve and retina.

The papillo-macular region sometimes retains its normal
colour and its functional activity, although the central artery
is completely occluded. This immunity is, doubtless, due to
the presence of small vessels — the so-called cilio-retinal — which
emerge from the temporal margin of the disc. In the few

THROMBOSIS OF THE VENA CENTRALIS RETINAL. 187

instances1 recorded in which these vessels have modified the
symptoms of embolism, they appear merely to have secured the
immunity of the part of the retina to which they were distributed,
and to have taken no part in establishing any collateral circulation
by anastomosing with branches of the occluded artery.

An example of this condition is seen in the case depicted in
Plate XLI., Fig. 93, which is now published for the first time.

Thrombosis of the Vena Centralis Retinae.

Thrombosis of the central vein has during recent years been
recognised as accounting for appearances of the fundus which were
previously attributed either to embolism of the central artery, or
classed as haemorrhagic or apoplectic retinitis. It is probable
that many cases described as haemorrhagic glaucoma were really
examples of venous thrombosis. The recognition of the pathology
of these cases is mainly due to the writings of Michel,2 Angelucci,3
and W. Wolf.4

We shall presently see that marked retinal changes result from
occlusion of the central vein. It might be thought that similar
symptoms would be produced by phlebitis of the cavernous sinus,
into which the ophthalmic vein opens. This, however, is not the
case. Thrombosis of the cavernous sinus commonly causes ophthal-
moplegia from implication of the nerves which lie in its wall, and
may also give rise to some proptosis from oedema of the orbital
cellular tissue. But, as a rule, no ophthalmoscopic signs are
present, and in the cases in which they have been observed it
is probable that the thrombus had extended down the ophthalmic

1 The following cases may be quoted : — Birnbacher, Ceutralbl. f. prakt. Augenli., Leipzig, 1883,
p. 207 ; Leplat, ibid., supplement to 1885, p. 489 ; Benson, Ophth. Hosp. Rep., London, vol. x.,
p. 340; Knapp, “ Ber. ii. d. Versamml. d. Ophth. Gesellsch.,” 1885, p. 219 (two cases); Schuller,
“Embolie der Art. cent, ohne Betheilung der macularen Gefasse,” 1888; Wadsworth, Trans. Am.
Oplitli. Soc., 1890, p. 672.

2 Arch. f. Ophth., Leipzig, vol. xxiv., ii., p. 37.

4 “ Ueber Thrombose der Retinalvenen.”

3 Ann. di. ottal, bd. ii., 1880.

188 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

vein. This immunity of the retina is due to the free communication
between the orbital and facial veins at the inner angle of the
orbit. This anastomosis, however, has dangers of its own, for it
enables facial erysipelas to cause thrombosis of the retinal veins,
as occurred in a case recorded by Knapp.1

Thrombosis may result from stagnation of the blood current,
or from changes in the vessel wall. In papillitis both these
conditions may be present, and it is possible that in some cases of
papillitis, in which the retinal veins are much distended and the
haemorrhages numerous, there is actually coagulation in the
central vein. But it is equally certain that thrombosis may
occur without any antecedent papillitis. Some of these cases are
possibly due to pressure on the vein from an atheromatous artery.
A more common cause is extension of a phlebitis of the orbital
veins.

Some of the results of venous obstruction have come under our
notice in dealing with optic neuritis. In thrombosis of the vein
these results are much more marked, because the obstruction is
more complete, its onset is more sudden, and there is not, as in
neuritis, simultaneous pressure on the artery. The retinal veins
become distended and extremely tortuous ; and the retina swollen
and possibly cedematous. Consequently the veins are seen to
make bold curves, the convexities of which stand out in relief,
while the concave portions are hidden in the substance of the
retina. The disc margins are indistinct or invisible, but the disc
itself is not generally much swollen. A striking feature is the
large quantity of blood that is extravasated, chiefly into the
fibre layer. It is most extensive round the disc over an area
having a radius of about 2 dd., where it may form an almost
uniform surface. Towards the periphery, also, there are numerous
haemorrhages, but they tend to be more scattered. Examples are
shown in Plate XXXIV., Figs. 76 and 77. In the following case
the diagnosis was confirmed post-mortem, : —

1 Arch. f. Augenh., Wiesb., bd. xiv., p. 257.

THROMBOSIS OF THE VENA CENTRALIS RETINAE. 189

Thrombosis of vena centralis — autopsy (Michel, Arch. f. Ophth., Leipzig, vol. xxiv.,
p. 2). — Peter M., ,58. Loss of vision of LE. discovered on waking (this previously was
the only useful eye). Seen within four clays. Ophthalmoscopic appearances almost
identical with those described above, and shown in Figs. 76 and 77. V. = counting
fingers. Marked sclerosis of peripheral arteries of the body. Emphysema of lungs. No
albumen in urine. There was some temporary improvement in vision, hut fresh retinal
haemorrhages subsequently occurred. Died from hydrothorax. A detailed description of
the microscopical appearances in the retina is given in the original paper. The following
are the most important points

Sections of the optic nerve showed a completely organised thrombus in the central
vein, about 6 mm. behind the globe. The ophthalmic artery and the cavernous sinus were
normal. In the retina the lumen of the arteries and veins free ; adventitia of arteries
somewhat thickened. The perivascular sheaths of tiie veins distended, and containing
lymph corpuscles, scattered in some places, and crowded in others.

In thrombosis of the central vein, loss of vision is generally
sudden, and for this reason some of the cases have been diagnosed
as embolism of the artery. The following table will serve to
contrast the ophthalmoscopic signs of the two conditions : —

Thrombosis of Central Vein.

1. Arteries, — calibre normal or slightly

diminished.

2. The veins are tortuous.

3. Veins turgid, and appear interrupted

(from being buried in retina).

4. Venous pulsation on pressure.

5. Extensive retinal haemorrhage.

Embolism of Central Artery.

1. Arteries filiform.

2. Course of veins normal.

3. Veins decrease towards the disc

(blood column may he broken into
segments).

No pulsation.

No haemorrhages, or very few.

In cases of retinitis, a single vein sometimes becomes greatly
distended and tortuous, while extravasations take place in the
portion of the retina drained by it. Such a condition is depicted
in Plate XXXVII., Fig. 83, and is probably due to thrombosis of
the affected vein. A case has been published by Wolf1 2 3 4 5 1 in which a
portion of a retinal vein, limited on either side by the crossing of
an artery, appeared empty, while on the peripheral side of the
obstruction, the vein was distended to three or four times its
normal calibre. The author attributes the obstruction in this case
to the pressure of the thickened arteries.

1 Loc. cit.

190 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

If the blocking of the vein is incomplete, haemorrhages may be
absent, and there may be no impairment of vision. It is possible
that some cases of uniocular optic neuritis, in which the signs
of venous obstruction are conspicuous, are due to thrombosis ;
Plate XXXIII., Fig. 75, may be an example of this. Although
the fundus changes were very conspicuous, vision was normal
throughout. The condition was attributed to a rather severe
blow on the temple. Fifteen months later all swelling of the disc
had disappeared. Its margin was clear, except above and below,
and a few grey bands of tissue in front of the centre of the disc
alone remained as evidence of the former papillitis.

Symmetrical Changes at the Macula in Infants.

This is an affection of the cerebro-spinal system, occasionally
seen in young infants, to which attention was first drawn
by Waren Tay.1 It causes changes at the macula somewhat
similar to those which result from embolism of the arteria
centralis retinae, but less extensive. Indeed, it seems probable
that this resemblance is more than accidental, and that the
changes at the macula are due to a failure of the circulation in
the extremities of the vascular loops, which converge towards the
fovea centralis (see Fig. 29, p. 66).

Although many points require further elucidation, the clinical
history of these cases is well established. It is briefly as follows : —

The disease has a tendency to attack several children in a
family at about the same age. At birth they are apparently healthy.
When they are a few months old, however, it is noticed that the
head cannot be held up, then it is discovered that the muscles of
the back and of the limbs are gradually losing power. There is
an entire absence of pain, and the child is not fretful — indeed, a
listless lethargic behaviour and an absence of crying appear to be
conspicuous. In some of the cases there has been optic neuritis

1 Trans. Oplitli. Soc., vol. i., p. 55, and vol. iv., p. 158.

SYMMETRICAL CHANGES AT THE MACULA IN INFANTS. 191

going on to atrophy, but in most, when the case was first seen,
the macula alone in each eye presented anything abnormal. It
is almost sufficiently descriptive of the condition of the macula
to say that it exactly resembles that seen in embolism. The
central region of the fundus is occupied by a soft white patch,
having a diameter of 15 to 2 dd. In the middle of this is the
typical cherry-red spot. It is evident that central vision is not
lost in the earlier stages, for the child fixes the light during
ophthalmoscopic examination in the persistent manner that is

Fig. 42. Fig. 43.

Warren Tay’s case of symmetrical change at the macula in infants (inverted).

common in young infants. It is possible, however, that the
fixation-point is surrounded by a wide belt of blindness,
corresponding to the white retinal area. The disease appears
to be invariably fatal, from progressive weakness.

There have been two autopsies recorded, and a microscopical
examination of the retina in a third case. The most complete is
that of Kingdon’s second case1 (No. 7 in the appended list of cases)
The child died at the age of one year, after having sunk into a

1 Trans. Ophth. Soc. vol. xii., p. 126.

192 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

weak, lethargic condition. “The symptoms during the last four
days reminded one of the attacks which occur during the later stages
of general paralysis of the insane.” Post-mortem — The posterior
fontanelle was closed, the anterior nearly so. Dura mater very
firmly adherent to the skull along the line of the superior
longitudinal sinus. No marked excess of cerebro-spinal fluid.
Sulci over whole brain appeared wider than usual. Arachnoid
and pia mater neither thickened nor adherent. No meningitis.

The brain was examined after hardening, but nothing abnormal
was detected in the primary fissures or convolutions. A large
number of sections from different cortical areas of the brain were
examined, and similar changes were found in all, viz. — the different
layers of cells were not so readily distinguished as usual. The
large pyramidal cells were, almost without exception, of a rounded
or oval outline. The cell substance did not stain well either with
methyl aniline blue-black, hsematoxylin and eosin, or acid fuchsin.
The protoplasm had lost its even granular appearance, and was
mostly collected into an irregular shrunken mass around the
nucleus, leaving large spaces between the contents and the wall
of the cell. The same changes were present to a less degree in
the small pyramidal cells. Deiter’s cells seemed to be largely
increased in number, but it was doubtful whether many of these
were not altered pyramidal cells. Sections of the spinal cord at
the second and third cervical vertebrae showed well marked
descending degeneration.

A microscopical examination of the eyes made by Mr. Treacher
Collins showed the choroid to be normal. In the central area
of the retina the only defect found was that the outer molecular
layer seemed spaced out and enlarged, as though there had been
some localised oedema. In both retina there was a prominent fold
in the macular region. A similar condition, it will be seen, was
present in case 8 {see p. 194).

The autopsy in the other case, which was under Dr. Knapp,
was less complete, since neither the spinal cord nor the eyes were

SYMMETRICAL CHANGES AT THE MACULA IN INFANTS. 193

examined. There was marked alteration in the large and small
pyramidal cells of the cortex, and atrophy of the cerebral con-
volutions from arrested cerebral development.1

The following is a summary of the cases hitherto recorded : —

Three cases in one family by Mr. Waren Tay (Trans. Ophth. Soc., vols. i. and iv.).

(1.) Eldest child (male). Seen at age of 12 months, when the typical ophthalmoscopic
appearances were already present.

When two or three weeks old the child was noticed to have little power of holding up its
head, or moving its limbs. The weakness increased, but at the time of the visit no paralysis
could be discovered.

Four months later child lying almost helpless. Changes at macula unaltered, but discs
becoming atrophic. Died at the age of a year and eight months.

(2.) Second child (male). Seen a few months after birth, with similar condition of the
eyes. Nothing amiss could then be discovered with the muscular or nervous system, but at
age of 6 months he began “to get weak all over,” like the first child. When 18 months old
admitted into London Hospital. Had convulsive seizures. One morning a definite epilep-
tiform convulsion, the right side of the body being rigid and the eyes deviating to the right.
The discs were atrophic, the yellow spots as in the first case. There were two other fits.
Child sank and died after being in hospital 24 days.

(3.) Third child of same family, also a male. When seen a few weeks after birth there

was optic neuritis, but no general weakness. At the age of 6 months the discs were

atrophic, and the typical macular changes were present. The child now appeared to be

beginning to fail like the first. The case could not be followed.

Two cases in another family by Mr. Waren Tay (Trans. Ophth. Soc., vol. xii.).

(4.) Male child, aged 11 months, lay helpless in mother’s arms. No power to lift his
head. Typical changes at each macula. Discs thought to be grey. Y. apparently defective.

Patient was sixth and youngest child.

(5.) The eldest child (male), said to have presented similar symptoms, he wasted and died
at the age of 15 months. Four other children — three females and one male — not affected.

Three cases in one family, by Mr. Kingdon (Trans. Ophth. Soc., vols. xii. and xiv.).

(6.) Eldest child, a male (born 1885), well developed at birth, subsequently became weak
in the back and limbs, was good tempered and apathetic, wasted and died at 2 years.

The second child, a girl (born 1886), was unaffected when seen at age of 5| years.

(7.) Second case, third child, a male (born October 1890). Seen at age of 8 months,
when typical changes were present in the eyes, as well as impaired movement of trunk and
limbs, and inability to hold up head. Child apathetic, seldom crying; evidently great
muscular feebleness. Changes at macula as in other cases. Child gradually became
weaker and died. The autopsy is given on p. 191.

A fourth child, a male (born April 1892), was seen when 10 days old, and again when
nearly 2 years old, and presented nothing abnormal.

(8.) A fifth child, female (born April 1893), (Trans. Ophth. Soc., vol. xiv.), was first seen

1 B. Sachs, Journ. Nerv. and Ment. Dis., N. Y., September, 1887.

194 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

when 3 months old. Muscular weakness was then commencing, but the fundi were
normal. When 5 months old there was a suspicious haze at each macula. When
8 months old the typical appearances were present at the macula. The child died, and
both eyes were removed and examined by Mr. Treacher Collins. His report, which has
not been published, is as follows : — -

The optic nerve is much atrophied. There is considerable increase in the amount of
the fibrous tissue between the bundles of nerve fibres, and also a large increase in the
number of round cells in the nerve. There is considerable cupping of the optic disc, due
to atrophy of the nerve fibres — almost down to the lamina cribrosa — and not to depression
backwards of that structure.

No inflammatory exudation is seen between the dural and pial sheaths of the nerve.
The central artery is full of blood clot ; the central vein is empty ; no alteration is seen in
the wall of either vessel.

The choroid in the region of the yellow spot has its vessels dilated, but no inflammatory
or other changes are seen in it. The retina at the yellow spot has a fold or ruck in it, so
that it is slightly detached in that region from the choroid. It is there much thickened,
due to enlargement of the outer molecular layer, the tissue of which is much spaced out,
here and there cavities being left ; the condition is apparently due to oedema.

So far as can be made out, the other layers show no changes. Elsewhere than in the
yellow spot the retina appears healthy.

(9.) Goldzieher ( Centralbl . f. prakt. Augenh., Leipzig, 1885, p. 219) mentions a case of an
infant with similar ophthalmoscopic appearance. The child died.

(10.) Magnus {Klin. Monatsbl. f. Augenh., Stuttgart, 1885, bd. xxiii., p. 42). Female child,
aged 18 months, the eldest. Muscles weak and flabby, unable to hold up head. Ophthal-
moscopic appearances at macula, as in other cases. Discs not atrophic.

(11.) Hirschberg {Centralbl. f. prakt. Augenh., 1888, p. 14) saw a feeble looking child
with similar condition of macula. It was said to be suffering from an incurable disease of
brain and spinal cord.

Two cases in one family, by Wadsivorth {Trans. Am. Ophth. Soc., 1887, p. 572).

(12 and 13.) Female, 11 months, sixth child. (The fifth, born four years before patient,
presented similar symptoms, and died at age of 18 months.) Child unable to sit, stand,
or hold tip her head. Muscles wasted. Fundi as in the other cases. Discs not well seen,
owing to persistent fixation of the light. Four and a half months later child did not fix
and discs were grey.

(14.) Case by Knapp {Ber. u d. Yjten Versamml. d. ophth. Gesellsch., Heidelberg, 1885,
p. 217). Seen when 4 months old. General condition improved. It then rapidly sank
and died at age of 2 years.

A post-mortem was obtained as already mentioned, but it did not include anexamination
of the eyes.

(15.) Female, 19 months (C. B. Carter, Arch. Ophth. and Otol., N. Y., vol. xxiii., p. 126),
second child. Eldest died at 7 months, after an illness of a week, “ with spasms.” Parents
were second cousins. Patient well till three months old. Then gradually increasing
weakness, without paralysis. When seen, unable to lift the head or to sit up. Limbs moved
slowly. Tonic contractions of muscles of neck and limbs every hour. Pupils active. Does
not follow a light. Changes at the macula as in the other cases. Discs pale six weeks later.
The discs were completely atrophic. Child died two weeks later. No autopsy.

LEUKJEMIC RETINITIS.

195

Leukemic Retinitis.

Marked fundus changes occur in the later stages of most
cases of leucocythmmia. Nor is this to be wondered at when
it is remembered how largely the appearance of the fundus
depends on the blood in the choroidal and retinal vessels, and
how profound is the alteration that the latter undergoes in this
disease.

In normal blood the proportion of white to red corpuscles is
one white to three or four hundred red. In the splenic vein the
proportion of white corpuscles is much higher, namely, one to
sixty or seventy red. In leucocythsemia, the number of white
corpuscles progressively increases, so that, in a late stage of the
disease, they may equal, or even exceed, the red. This alone is
sufficient to alter appreciably the colour of the blood when seen
in bulk, or in the blood vessels of a tissue as vascular as the
choroid, and explains the pale yellowish or orange tint which the
fundus presents in some of these cases. The white corpuscles
are larger than the red, and they have a decided tendency, not
shown by the latter, to dawdle along the wall of the vessel, or
even to remain in contact with it. This tendency, together with
their accumulation in the vessels, seriously impedes the circulation.
There can be no doubt that most of the fundus changes are due
to this cause.

The most constant and conspicuous of these changes is the
enormous distension and tortuosity of the retinal vessels. The
arteries may be affected to an extent only slightly less than the
veins, and, as the change in the blood tends to diminish the
difference in colour between the two sets of vessels, it is sometimes
difficult to distinguish between them.

A less constant ophthalmoscopic appearance is produced by the
presence of small, rounded, white spots, chiefly at the periphery ;
the larger of which are raised above the level of the retina. They

196 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

probably consist of leucocytes which have escaped from the
overfilled capillaries (Gowers). In other cases there are white dots
which are due to degeneration of the tissue of the retina.

In leucocythsemia there is a strong tendency to haemorrhage, as
shown by the frequent co-existence of epistaxis, and bleeding from
the alimentary canal, and by profuse haemorrhage following slight
wounds. Notwithstanding this tendency, retinal haemorrhage,
although sometimes extensive, is by no means a constant symptom.

Lymphatic deposits occur in many organs. In a remarkable
case, published by Leber,1 such growths were present in all four
eyelids, and, as he believed, from the great proptosis, also in the
cellular tissue of the orbits.

Fig. 44. — Leukaemic retinitis.

a. Sclerotic ; b, choroid ; c, retina.

An illustration of the ophthalmoscopic appearance that may be
present in this disease will be seen in Plate XXXIII., Fig. 74.
The veins and arteries, especially the former, are enormously
distended, make snake-like curves, and are similar in colour. It
is to be noticed that the light-streak on them is unusually con-
spicuous. The whole fundus has an indistinct appearance as if
veiled by some cloudiness of the media, although no definite
opacities were visible.

1 Arch. f. Ophth., Leipzig, bd. xxiv., ab. i., p. 295.

LEUKEMIC RETINITIS.

197

The patient from whom this drawing was made died six
weeks later. Mr. John Griffith examined the eyes post-mortem,
and kindly favoured me with the following report, as well as with
the microscopical section from which Fig. 44, p. 196, is drawn : —

Post-mortem on January 30th, 1893. Both eyeballs, with optic nerves, were removed
intact. After being hardened in Muller’s fluid for about six weeks, the LE. was used for
making a “jelly preparation,” and the RE. was used for microscopical sections.

The papilla was slightly swollen, and the retinal vessels, especially the veins, like the
vessels in all parts of the globe, were gorged with leuksemic blood.

The changes in the retinal vessels, as described and depicted by Mr. Edmunds {Trans.
Ophth. Soc., London, vol. x., p. 157), were not present.

The walls of the blood vessels were normal, and all the vessels contained blood (not
coagulum), in which the leucocytes appeared to predominate. The choroid showed this
vascular distension in a remarkable manner, being two or three times its natural thickness.

Contrary to what might be expected, there was no excess of leucocytes in the
perivascular tissue ; in fact, it appeared as if diapedesis had been thrown into abeyance.

The ciliary processes and iris were slightly swollen, but were otherwise normal.

The optic nerve, at its junction with the globe, was somewhat bulbous, but there was
no excess of cellular elements in the inter-sheath space. The optic nerve itself showed no
signs of inflammation, the swelling being due, as I believe, entirely to mechanical oedema of
the papilla, which obstructed the venous return.

In a case published by Oeller,1 the changes in the choroid and
retina were more advanced. Unfortunately no ophthalmoscopic
examination had been made. The following is a greatly abridged
account of the conditions found post-mortem : —

Spleen much enlarged. A great accumulation of leucocytes not only in its vessels, but
in their sheaths, and throughout its parenchyma. In the liver and lungs the vessels, even
to their finest branches, choked with leucocytes. In the eye the choroid was in places
double the normal thickness, and contained leucocytes so crowded together that it was
impossible to ascertain whether they were in the vessels or free in the tissue. The larger
vessels were enormously dilated, and most of them were filled with blood corpuscles in the
proportion of from six to ten white to one red ; only in a few did the red preponderate.
In other situations there were no free corpuscles, but the choroidal vessels were filled with
them, the white preponderating. The head of the optic nerve was moderately swollen.
In the nerve itself there was an excess of nuclei, and the interstitial tissue was increased.
In the retina the fibre and nerve cell layers were nearly double the normal thickness ; the
layer of rods and cones were much atrophied. The retinal vessels dilated, and very
tortuous, and from them capillaries (new ?) could be traced as far as the outer granular
layer.

1 Arch. f. Ophth., Leipzig, bd. xxiv., ab. iii., p. 239.

198 AFFECTIONS OF THE VASCULAR SYSTEM OF RETINA.

In a case recorded by Walter Edmunds,1 the walls of the
retinal arteries were much thickened, and the endothelium
proliferated, the veins were filled with clot, containing an excess
of leucocytes, but their walls were not thickened.

We have seen that many pathological changes in the optic
nerve and retina depend upon general conditions. Thus, they may
be associated with diseases of the central nervous system, with
changes in the character of the blood, or with affections of the
heart or kidneys.

The importance of vision in all the occupations of life leads
patients who suffer from its deterioration to seek advice earlier than
they might do on account of general symptoms. Hence those who
practice ophthalmic surgery have the first opportunity, in many
cases, of recognising general conditions of grave import to health
or even to life. Opportunities of this kind are, however, useless,
without sufficient knowledge of medicine in general. To the
physician, on the other hand, the ophthalmoscope frequently lends
valuable aid in forming a diagnosis, or in determining a prognosis.
It will, however, prove a misleading guide if he has not had
sufficient experience in its use to be familiar with the more common
physiological variations of the disc and fundus.

In the conditions of the retina which remain to be considered,
the connection with general disease is less direct or less obvious.

1 Trans. Ophth. Soc., vol. x., p. 157, and Figs. 1 and 2, Plate VI.

CHAPTER XI.

PUNCTATE CONDITIONS OF THE FUNDUS.

Several conditions resemble each other in presenting a number
of pale dots scattered over the fundus. None of these are larger
than the width of the primary divisions of the retinal vessels, and
some are much smaller.

Some of these dots doubtless originate in the choroid, and
subsequently invade the retina, or, at any rate, its pigment layer.
It is equally certain, however, that others are of retinal origin.
Our knowledge is not yet sufficiently advanced to permit us
to make a complete classification, but we may conveniently
include these conditions under the designation of punctate
conditions of the fundus, and consider them under the following
heads : —

(a) The dots described by Marcus Gunn, and called by
his name, have already been described (p. 26). They are of
small size, occur chiefly in the yellow spot region, and are
arranged in groups. The usual mode of arrangement is seen in
Plate IV., Figs. 9 and 10, and Plate XI., Fig. 30, but the dots
never appear so conspicuous as this ; indeed, one of their chief
characteristics is that they are difficult to see, being often visible
only when the light is feeble, and falls on them obliquely. Their
colour does not approach whiteness, they are merely a paler
colour than the fundus, sometimes having a yellowish tinge.
They are most frequently seen in the dark eyes of young subjects
in whom the retinal reflexes are well marked.

(b) Minute silvery dots are occasionally seen. Unlike the
preceding variety, they do not occur in groups, but are isolated.
They are so small that they would easily be overlooked, were

200 PUNCTATE CONDITIONS OF THE FUNDUS.

it not for their great brilliancy, which gives them a metallic
appearance, like particles of mercury. They may be met with
at any age, and, although more frequently seen between the
disc and the fovea centralis, they may occur in any part of the
fundus. The writer has most frequently seen them in cases in
which the ophthalmoscope has been used with especial care to
ascertain the cause of an unexplained amblyopia. But they are
also found in eyes with normal vision. They are too small and
round for crystals of cholesterin, and are probably due to some
irregularity of the retinal surface, which causes total reflection
to take place, the metallic brightness being produced by the
image of the ophthalmoscope mirror. Their brilliancy of reflection
suggests the term metallic dots.

(c) The dots of chalky whiteness which are often seen in the
yellow spot region in cases of neuro-retinitis have already been
sufficiently described in dealing with that condition.

(i d ) Isolated dots, few in number, and of white colour, are
occasionally seen in the eyes of persons past middle life. Hyaline
excrescences projecting from the lamina vitrea of the choroid into
the retina are known to occur in such eyes, and the appearance
is attributed to them.

(e) According to Nettleship,1 a condition of the fundus occurs
in young persons, in which the spots are small, round, and
dead white in colour. They usually lie between the macula
and the periphery, the macula itself being free. He has
met with the condition in several members of the same family,
in whom it was associated with night blindness and contraction
of the visual fields. At the periphery of the fundus, beyond
the area occupied by the white dots, were pigment changes,
consisting in a mottled appearance of the pigment layer,
and, in some instances, in deposition of pigment, which, how-
ever, had not the typical arrangement characteristic of retinitis
pigmentosa.

1 Trans. Ophth. Soc., vol. vii., p. 301 ; and vol. viii., p. 163.

“ TATS CHOROIDITIS.”

201

The peripheral pigment changes and the subjective symptoms
might be thought to point to the condition being a variety of
retinitis pigmentosa. But against this is the fact that in two
sisters who were seen by Nettleship1 after an interval of five
years, no appreciable change had occurred. True retinitis pig-
mentosa, however, occasionally appears to remain stationary for
many years. The cases, therefore, would have to be watched for
a long period before any positive conclusion could be arrived at.
A mottled condition of the fundus at the periphery is sometimes
seen as a result of inherited syphilis, but there were no definite
signs of this disease in any of the cases.

These cases are considered by Nettleship to be identical
with one described by Mooren 2 under the title retinitis punctata
albescens.

(/) The next group of cases has been described under a variety
of names, a glance at which will indicate that they represent
different views as to the pathology of the affection under con-
sideration. The following are some of the terms used : — “ Tay's
choroiditis/' 3 “ Infiltration vitreuse de la re tine (Masselon) ” 4
“ Punctate retinitis,” “ Central senile guttate choroiditis.”

The common characteristics of these cases are that the dots
are round, pale yellowish, about the diameter of the primary
retinal arteries, and occur chiefly in the central region of the
fundus. They are met with, as a rule, only in persons past
middle life, and, unless very numerous, do not cause serious
impairment of vision.

A typical example of this condition is given by Nettleship,5
whose paper is illustrated by an excellent chromo-lithograph. In
Masselon's monograph also there are some good photographs.

Owing to the extreme slowness with which the condition
changes, and to the fact that vision is not much affected, little

1 Trans. Ophth. Soc., vol. xiii., p. 292. 4 Masselon, “Infiltration vitreuse de la retine,” 1884.

2 “ Fiinf Lustren,” 1882, p. 216. 5 Trans. Oplith. Soc., vol. iv., p. 162.

3 Ophth. Hosp. Rep., London, vol. viii., p. 231, 1875.

202

PUNCTATE CONDITIONS OF THE FUNDUS.

is positively known about the progress of these cases. It is
probable, however, that eventually further degenerative alterations
occur, leading to atrophy of the central part of the choroid.

(g) Dots resembling those of Tay’s choroiditis are sometimes
met with in the eyes of younger persons (Plate XI., Fig. 31),
but in these cases they are much more numerous, and are not
limited to the macular region. The condition remains without
appreciable change for many years, and is not, as a rule, associated
with any impairment of vision, although in some cases there has
existed a slight degree of night blindness, and in a few slight
contractions of the visual field. The condition is probably due to
some change in the pigment layer, possibly a colloid degeneration
such as described by Wedl and Bock.1

Under the term colloid disease of the macular region, G. de
Schweinitz 2 has described a grouping of these dots in the macular
region. They were closely aggregated, and covered a circular
area of about three disc diameters. In the illustration given by
the author the dots appear very similar to those in Plate XI.,
Fig. 31, but they are described as having a raised appearance, and
seeming in places to be piled one above the other.

It is at present doubtful whether these cases should be
considered to constitute a separate group, or should be included
in the class described by Nettleship, which have been con-
sidered under ( e ), or finally, if they represent a variety of Tay’s
choroiditis.

The following list shows the main characteristics of the different
varieties of punctate conditions : —

Summary of Punctate Conditions.

(a) Gnnrts small dots. — Pale or yellowish, in groups in Y.S. region. Difficult to see.
Chiefly in young eyes.

(b) “ Metallic ” dots. — Minute, isolated. Occur in any part of fundus. Conspicuous
from their brightness. Occur at all ages.

1 Path. Anat. des Auges., p. 219, and Fig. 100.

2 Trans. Am. Ophth. Soc., 1894, p. 212.

HYALINE PROLIFERATIONS ON THE DISC.

203

(c) Neuritic dots. — Irregular shape. Chalky whiteness. In Y.S. region, and between
this and OP. Associated with signs of neuro-retinitis.

(d) Hyaline excrescences from lamina vitrca. — Isolated white round dots. Usually in
old persons.

(e) Nettleship’s dots. — Minute, dead white, round. Numerous, uniformly scattered
between macula and periphery. Associated with pigment changes at periphery and night
blindness. Occur in several members of same family. Stationary or very slowly
progressive.

(/) Tag’s choroiditis. — (Central guttate choroiditis. Infiltration vitreuse de la retine.)
Pale or yellowish, approaching whiteness. Scattered chiefly Y.S. region. Occur after
middle life.

(y) Colloid change in pigment layer. — Numerous pale dots, almost in contact. Occurring
over whole fundus. Most numerous in Y.S. region. No impairment of vision. Met with
in young adults.

Hyaline Proliferations on the Disc. (Syn. Amyloid
Bodies, Drusenbildungen.)

Clusters of small, glistening, globular bodies are occasionally
seen on the disc. They are highly refracting, of grey or bluish-
grey colour, and are closely aggregated, like an unthinned bunch
of grapes.1 They have generally been considered as being of the
same nature as the outgrowths from the lamina vitrea of the
choroid, and, as they are most commonly situated on the margin
of the disc, it has been thought that they are connected with that
structure. Microscopical examination, however, of two papillse, in
which these bodies had been seen with the ophthalmoscope 2 has
shown that they may also be present in the nerve behind the
lamina cribrosa. They would appear, from this case, to be com-
posed of a material almost identical with the hyaline substance
sometimes met with in the outer coat of the blood vessels, and
to result from a degenerative change in the interstitial tissue of
the nerve and papilla. The condition does not appear to cause
any impairment of vision, unless the nerve fibres are pressed upon.

1 For two excellent illustrations of the ophthalmoscopic appearances see Nieden, Arch.
Ophth. and Otol., N. Y., vol. xviii., p. 198.

2 Sachsalber, Beitr. z. Augenh., Hamb. u. Leipzig, heft xxi., 1895.

CHAPTER XII.

PIGMENT CHANGES IN THE RETINA.

Pigmentary Degeneration of the Retina — Retinitis
Pigmentosa — Sclerosis of the Retina.

Under these various names has been described a disease, which
has usually a definite clinical history, and which presents a
characteristic ophthalmoscopic appearance, although many points
in its pathology are still obscure.

The first symptoms manifest themselves, as a rule, about
puberty ; exceptionally, however, the disease is found to be
already considerably advanced in childhood. These latter cases
are usually regarded as examples of the congenital form of the
disease.

The most noticeable subjective symptom is usually night-
blindness ; that is, a disproportionate lowering of the visual
acuity under reduced illumination. This may be so pronounced
that a patient who is not conscious of any defect in broad daylight
may require to be led by the hand at dusk, or on going in the
daytime into a badly lighted room.

Night blindness also occurs in other affections, especially in
cases of advanced choroido-retinitis in which there is much
atrophy of the pigment layer. Occasionally it is absent, or at
least not prominent, in cases of retinitis pigmentosa, which are
otherwise typical. That it depends neither upon the severity of
the disease, nor upon the stage in which it is seen, appears from
a case published by Hutchinson,1 in which this symptom was
absent, although the disease had existed for twenty years, and
the ophthalmoscopic signs were well marked.

1 Ojphth. Hosp. Rep., London, vol. vi., p. 39.

RETINITIS PIGMENTOSA.

205

A nearly constant symptom is concentric contraction of the
visual field. Of this the patient is usually unconscious, although
he describes vividly enough its direct consequence, namely, that in
walking towards a point on which his gaze is fixed, he knocks
against intervening objects.

The fundus changes in retinitis pigmentosa are characteristic,
but in the early stage they may easily be overlooked, since they
are then limited to the periphery. The most noticeable is the
deposition of pigment in the superficial layers of the retina. At
first the pigment is seen only towards the equator, and may be
limited to a few branching streaks, or dots with processes shooting
out from them (as in Plate XLIV., Fig. 97). As the pigment
become more abundant, it forms an irregular network, as in
Plate XLII., Fig. 94. If examined closely, it is now seen to
consist for the most part of irregular spots of pigment with
processes jutting out and anastomosing with similar branches
from other spots. The appearance presented by the pigment
deposits has been compared with that presented by bone-
corpuscles under the microscope. A comparison with moss,
teased out and flattened, would be more accurate. The pigment
often invades the sheath of a blood vessel, and may then conceal
the blood column for a short distance. Under the microscope,
vessels too small to be visible with the ophthalmoscope, are found
thus encased in pigment, and the appearance presented to the
ophthalmoscope of black branching lines (as in Plate XLY.,
Fig. 97) sometimes suggests that the pigment may be lying in
the course of vessels which are too small to be visible. There is,
however, no known anatomical arrangement of the fine vessels
which enables us to accept this as the explanation of the
arrangement of the pigment when it is abundant, as, for example,
in Plate XLII., Fig. 94.

In choroiditis the distribution of the pigment is, as already
pointed out, quite different. It encircles or covers the areas of
choroidal exudation, so that when the latter has been absorbed the

206

PIGMENT CHANGES IN THE RETINA.

pigment remain in the form of rings or discs as in Plate XV.,
Fig. 40 ; and Plate XVIII., Fig. 44. It must, however, be
remembered that in a late stage of choroiditis secondary
pigmentation of the retina may occur, and produce a condition
identical with retinitis pigmentosa.

Both in choroiditis and in retinitis pigmentosa the source of
the pigment is the pigmentary layer of the retina, which, it will be
remembered, lies next the choroid. The stellate arrangement
of the pigment deposit which characterises retinitis pigmentosa
only occurs when pigment has reached the surface of the retina.
To do this it must traverse all the retinal layers, and it is
probable that degenerative changes in these are a necessary
preliminary to its passage.

In the early stage of retinitis pigmentosa the symptoms are
night blindness and some contraction of the visual field in each
eye. The ophthalmoscopic changes may be limited to the
equatorial zone, and consist of only a few streaks or dots
of pigment. Sometimes normal fundus can be seen at the
periphery beyond the affected zone. The portion of the visual
field that is lost is always greater than would correspond
with the pigmented area of the retina. Consequently, even
when there exists a peripheral zone of healthy fundus, the
periphery of the field is usually lost. In exceptional cases,
however, of this nature, the defect in the field consists in a
band corresponding in position with, but wider than, the band
of pigment. Such a condition is called a ring scotoma. In the
description facing Plate XLII., Fig. 94, is seen the chart of a
field, in which such a ring scotoma appears to be in process of
formation.

The advance of the disease is shown by increase in the amount
of pigment, which slowly creeps towards the central region, and
by progressive contraction of the fields. Central vision, although
usually eventually impaired, may long remain unaffected in a good
light. It is usual, as the area of pigment deposit increases, for the

RETINITIS PIGMENTOSA.

207

pigment layer to undergo some atrophy, so that the choroidal
vessels become visible.

In advanced cases, as Plate XLIII., Fig. 96, there are other
changes which indicate degeneration of the retinal tissue. The
width of the blood column in both the arteries and the veins
becomes reduced, and the disc assumes a dull greyish appearance.

The change in the vessels is due to a hyaline thickening of
their walls, which encroaches on the lumen. It does not
interfere with the transparency of the vessel wall ; the blood
column, therefore, remains visible, but may be reduced to a
mere thread.

The change in the disc occurs not only in retinitis pigmentosa,
but in some cases of old choroiditis. Although easily recognised,
it is difficult to describe or to depict. The term waxy is often
applied to it, but a comparison to old parchment would perhaps
be more appropriate. Its surface looks dull and flat, as if its
transparency were impaired. Its colour is pale grey, with a
yellowish tinge. The margin may look a little hazy, probably
from impaired transparency of the nerve fibres, but there is an
entire absence of any swelling. Sometimes it is surrounded by a
halo of choroidal atrophy.

Posterior polar cataract occasionally develops, but less fre-
quently than in choroiditis.

The progress of the disease is very slow, and the ophthalmo-
scopic appearances often present no appreciable alteration after an
interval of three or four years. The night blindness, however,
usually increases.

It is evident from what has been said that the deposition of
pigment, although giving a name to the disease, is not the only
tissue alteration in the retina. Indeed, there is good reason for-
believing that the pigmentation of the retina is merely secondary
to other changes, and is not an essential feature of the morbid
process. In the first place, the amount of pigmentation stands
in no constant relation to the duration of the disease or to the

208

PIGMENT CHANGES IN THE RETINA .

degree of visual impairment. Secondly, pigmentation, identical
with that of retinitis pigmentosa, may occur as a secondary
change in any condition which has caused atrophy of the retina
with great diminution of its vessels. It also occurs in animals
after experimental division of the optic nerve. Lastly, cases are
occasionally met with which exhibit most of the symptoms of
retinitis pigmentosa, but show no deposition of pigment.

The above facts point to the process being degenerative
rather than inflammatory, and it is strange, therefore, that it
should usually commence in early life. Indeed, the etiology of
the disease is involved in obscurity. Its typical form does not
seem to depend upon inherited syphilis, although Loring states
that there is a form of the disease due to this cause, and that it
affects one eye only. This is so opposed to what we know of
syphilitic affections that the statement requires corroboration.

The writer has seen an affection of the pigment layer in
syphilitic children, which produced in the periphery of the fundus
a mottled appearance, with numerous small pale, but not very
conspicuous dots, possibly due to a colloid degeneration of the
pigment cells, but the cases were not under observation sufficiently
long for the subsequent stages to be followed.

Consanguinity in the parents is believed by many authorities
to be a frequent cause of retinitis pigmentosa. It is difficult to
estimate the truth of this without knowing the proportion of these
to other marriages. It is certain, however, that in this country only
a very small proportion of the cases of retinitis pigmentosa are the
offspring of marriages of consanguinity. The disease usually affects
several members of the family, and is hereditary to a marked
degree. The liability to it would doubtless be greatly increased by
intermarriages between members of a family in which it existed.

Retinitis pigmentosa occurs in a large proportion of deaf mutes,
but the cause of this association is unknown.

A degenerative process, which might be called choroido-retinal
sclerosis, is sometimes met with in the adult fundus. It produces

RETINITIS PIGMENTOSA.

209

appearances in some respects resembling retinitis pigmentosa, and
is usually accompanied by similar symptoms. There is deposition
of pigment in moss-like masses, but these are fewer and more
isolated than in retinitis pigmentosa. There is atrophy both of
the pigment layer and of the capillary layer of the choroid, so that
the choroidal vessels are visible, and the spaces between them are
of chocolate colour. In a late stage of the disease, the choroidal
vessels, especially near the disc, become white. These changes are
probably secondary to diffuse choroiditis, and have been described
more fully with that condition on page 106 (for examples, see
Plate XXVI., Fig. 60, and Plate XXVII., Fig. 61).

Pigment Streaks on the Fundus. (Syn. Angioid Streaks.)

Pigment derived from the pigment layer of the retina tends to
arrange itself, as we have seen, in the form of branching spots,
forming an open network in retinitis pigmentosa, or in thicker
lines bordering a patch of choroidal atrophy, or more rarely in
large masses in choroiditis. In all these cases the pigment is
black.

Cases have been described which differ from all these, in the fact
that the pigment is not black, but of a dull red brown, like the
pigment moles described on page 19. It is arranged in long
irregular streaks, which in respect of their size, mode of branching,
and course, somewhat resemble blood vessels, but their borders are
irregular and jagged, their diameter variable, and the bends that
the streaks make are more angular than is usual in blood vessels.
Moreover, no direct connection can be traced between them and
the vessels of the choroid or retina.

The writer is acquainted with six published cases, which,
although they present differences of detail, are sufficiently similar
to warrant the conclusion that they are identical in nature.

In all, both eyes were affected. In Mr. Doyne’s patient there
was a history of an injury to each eye ; there was considerable
27

210

PIGMENT CHANGES IN THE RETINA.

choroidal or retinal hsemorrhage in the one eye, and the history
pointed to its having occurred in the other. In some of the
other cases, the history of sudden failure many months before the
ophthalmoscopic examination, and the presence of small extravasa-
tions, point to the probability of a haemorrhagic origin.

Fig. 45. — Mr. Doyne’s case of retinal streaks.

The following is a brief summary of these cases 1 : —

(1.) Ottilie K., young adult (Knapp, Arch. Ophth. and Otol., N. Y., bd. xxi., p. 289, 1892). —
Taken ill in 1889 with vomiting and diarrhoea, five days later sudden pain and dizziness in

1 All the published accounts are accompanied by illustrations. The last three by chromo-
lithographs, which give a good idea of the appearance of these streaks, and the first by a drawing in
black and white, which shows their distribution.

PIGMENT STREAKS ON THE FUNDUS.

211

eyes, following exposure to bright light. Then gradual deterioration of V. When seen
three months after commencement of illness, both OR’s. white, fields contracted, vessels of
normal calibre. Fundi dull and mottled. A month after first visit choroidal pigment
showed disturbance, and there was seen a system of dark-brown or black streaks lying
beneath the retinal vessels, radiating in every direction from the neighbourhood of the disc,
their diameter was irregular. No haemorrhages seen, but some of the streaks had red
portions. Eighteen months later no material change but the red portions of the streaks
had disappeared.

Fig. 46. — Mr. Stephenson’s case of retinal streaks.

(2.) Mrs. H.,83 (Plange, ibid, p. 282). — In 1879 she noticed a failure of vision. There
was a transient improvement, but in the course of years V. failed again. When seen, the
condition noted was as follows : —

Brown membranous filaments in each eye, about diameter of retinal vessels. They were
2-3 dd. long, and ran in the general direction of the vessels. At the peripheral end of each,
a small haemorrhage. In RE. three such striae united at the nasal side of disc. Another
filament ran to YS. from opposite side of OR., and ended in a white atrophic plaque which
included the macula. In the L. a single pigment stria running up and in from nasal side of
OR. and ending in a haemorrhage. Patient was watched for six months, during this time

212

PIGMENT CHANGES IN THE RETINA.

the haemorrhages in RE. partially absorbed and recurred several times, the membranes
developing as the haemorrhages underwent absorption.

When seen ten years later, the following was the condition : — RE. dull-brown streaks
radiating from the disc. Their origin near the disc is not sharply defined, hut they appear
to proceed from a layer of opaque greyish-white glistening tissue, they are here double the
diameter of the central vessels, towards periphery they become narrower and break up
into a number of plaques and points of the same colour. The striae are included in broader
bands of lighter colour, which give the appearance of retinal reflex. A patch of atrophic
choroiditis at YS. Y. finger eccentrically at 3 M.

LE. four main pigment striae run from neighbourhood of OD. towards periphery ; they
are about the size of the primary retinal veins ; near the disc some give off communicating
branches which, uniting, form an incomplete circle round the disc. Y. normal.

With a few exceptions the striae are depicted in both eyes as lying beneath the retinal
vessels.

(3.) Male, name and age not stated. (Doyne, Trans. Ophth. Soc.. vol. ix., p. 128). — More
than ten years ago, an injury to LE. followed by loss of central vision. This recovered
and when seen V. •§-.

Six weeks ago, blow on RE. Central vision lost. An extensive choroidal haemorrhage
which is clearing up, leaving patches of atrophy. In both eyes pigmented lines radiating
from the disc. In the eye depicted (Fig. 45, p. 210) they are mostly accompanied by white
bands ; their outline is jagged and irregular ; they are coloured grey, some being reddish-
brown. They all lie beneath the retinal vessels. Most of the lines run in a radial direction
from OD., but they are connected near OD. by similar small lines parallel with disc margin.

(4.) Samuel G-., 42 (Stephenson, Trans. Ophtli. Soc., vol. xii., p. 140). — About fifteen
months before he was seen the left eye began to fail. After deteriorating for three to four
weeks the sight again improved. Three months before he was seen both eyes failed, the
left being the worse. The sight continued to deteriorate up to the time of his visit.
There was a systolic murmur, believed to be mitral, otherwise the patient appeared to be in
good health. The ophthalmoscopic appearances were similar in the two eyes. Those in the
left eye are shown in Fig. 46, p. 211. Brownish-black ragged branching lines radiate from
the disc, a few are accompanied by white bands. They all lie beneath the retinal vessels.
A few small haemorrhages, and a patch of cicatricial tissue, with concave borders at YS.
Later, fresh haemorrhages occurred.

(5.) Josephine P., 23 (Walser, Arch. f. Augenh., Wiesb., vol. xxxi., p. 345, 1895). — In RE.
a broken line of pigment surrounding the disc and lines radiating from it. The lines were
grey, with a tinge of brown, and their outline was jagged. They lay on a deeper level
than the retinal vessels. Some accompanied by white lines. Y. = f. ISTo history of injury.
LE. presented a similar condition.

(6.) Johan M., 22 (ibid.). — The ophthalmoscopic appearances were similar to those in
the preceding case, and were present in both eyes. Y. = £. No history of injury. Drawings
are given of both cases.

CHAPTER XIII.

DETACHMENT OF THE RETINA.

An old standing detachment of the retina presents an ophthal-
moscopic appearance so striking and characteristic that its
recognition is easy, but in an earlier stage, while the retina is
still transparent, the diagnosis is more difficult.

The term detachment is generally limited to cases in which
the retina is separated from the choroid by fluid, but a somewhat
similar appearance is occasionally produced by oedematous or
other thickening of the retina itself. The retina may be
mechanically pushed forward by a choroidal tumour ; in such
cases there is generally, in addition, a larger area of secondary
detachment, beneath which there is fluid.

Although it is not proposed to discuss fully the pathology
of retinal detachment, with regard to which many points are
still undetermined, there are certain mechanical conditions which
must be borne in mind in any consideration of the subject.

If a recently excised eye is bisected and examined, it will
be seen that, while the choroid adheres rather firmly to the
sclerotic, the retina, on the contrary, can hardly be said to be
attached at all, except at certain points, for it can readily be
lifted up with a pair of forceps. The adherent parts are
the optic papilla, where the retinal nerve fibres and those of
the optic nerve are continuous, the ora serrata, and the macula
lutea. Between these points the retina is kept in contact with
the choroid merely by the pressure of the vitreous. Another
factor to be considered is the rigidity of the sclerotic, while the
retina is so flexible that it readily falls into folds, and is, besides,
very easily torn.

214

DETACHMENT OF THE RETINA.

A consideration of these facts will show that if there occur a
sudden diminution in the pressure exerted by the intraocular
fluids, — as, for example, by vitreous escaping through a wound,
there will be a tendency for the retina to fall away from the
choroid. As long, however, as no fluid finds its way between
the two membranes, they will remain in contact, but if the
retina should tear, or if fluid should exude from the choroidal
vessels, detachment of the retina will at once take place.

Conditions produced thus suddenly by accident may be
established more gradually by disease. In the late stage of many
morbid conditions the vitreous becomes unnaturally fluid and
reduced in volume ; detachment will then occur as soon as a rent
in the retina admits fluid from the vitreous, or as soon as
exudation takes place from the choroid.

This explains how it is that although the disease is chronic,
detachment usually occurs suddenly. Gradual detachment might
occur without any rent in the retina, if pari passu with the
shrinking of the vitreous, subretinal exudation occurred, but the
clinical history in most cases points to a sudden occurrence of
detachment.

In cases of choroidal tumour the process is probably similar,
though here the force acts by a push from behind instead of by a
pull in front : the retina resists separation till its tissue tears, then
there is extensive floating up.

It was formerly held that most cases of detachment were
caused by subretinal exudation. To Nordenson1 we owe the
modern theory of vitreous traction, with which the clinical facts
are entirely consistent. Detachment usually occurs, apart from
traumatic cases, in eyes of low tension. It is nearly always
accompanied by opacities in the vitreous, which in many instances
are known to have existed prior to the occurrence of the detach-
ment. Where a blow on the eye causes detachment, without

1 “Die Netzhautablosung,” 1887.

MYOPIA AND DETACHMENT.

215

producing an external wound, there is probably always a tear of
the retina.

Eyes which are highly myopic are especially prone to detach-
ment. In such the vitreous is usually unduly fluid, and often
contains opacities. Apart from the state of the vitreous, it
is not easy to see what is the connection between myopia and
detachment. At first sight it might seem that the increasing
volume of the globe might lower the intraocular tension, but the
continuous enlargement of the globe must be due to the resistance
of the sclerotic being less than the pressure of the intraocular
fluid, and if the latter became less the globe would cease
to enlarge. The increased bulk of the vitreous, however, in these
cases is probably made up by fluid, and as the rate of absorption
and secretion may vary with conditions of the general circulation,
it is quite possible that there may be greater fluctuations in the
intraocular tension than in the normal condition, and that
detachment takes place during a temporary lowering of the
tension.

At the moment of detachment the patient is frequently
conscious of a corresponding loss in the visual field, and usually
throughout the case the detached portion of the retina remains
blind. Exceptionally, however, the defect in the field is smaller
than would correspond with the detachment ; and the defect
may even escape notice altogether if the examination be conducted
in a good light. It is probable that in a subdued light a deficient
area would always be discovered.

In some cases the vision, and probably, also, the extent of the
detachment, vary from time to time, and it is quite common for
patients to say that they are much better on first rising in the
morning.

We now turn to the ophthalmoscopic appearance presented by
detachment. In old standing cases this is so striking that the
diagnosis is easy, for the detached retina becomes opaque, and is
conspicuous from the white reflex which it affords (Plate XLVI.,

216

DETACHMENT OF THE RETINA.

Figs. 102, 103). Indeed, such a detachment can only escape
observation by the surgeon failing to carry his examination
sufficiently towards the periphery.

The optical conditions of the detached portion are those of
the fundus of an extremely hypermetropic eye. That is to say,
it can be seen from a distance, and if looked at with the
ophthalmoscope close to the eye, it can be focussed with a
strong convex lens. Its details are then seen with great
clearness. The surface is thrown into numerous irregular folds
which are approximately parallel. The summits of these reflect
the light from the mirror, and often look like white lines ; the
furrows between them, on the other hand, are in shadow and
are consequently less conspicuous. The vessels follow the folds
of the retina. They often appear darker than normal, the
central light-streak is absent, and they always look small, like the
vessels in hypermetropia. The dark colour is probably due to
contrast and the absence of the light streak ; the small size, of
course, depends on their being less magnified by the dioptric system,
owing to the retina being well in front of its focus. The absence
of the light streak is less easily explained, but possibly it depends
upon the plane of the retina not being perpendicular to the line of
vision, as in the normal condition.

When the detached retina is transparent the diagnosis is less
easy. Hence these cases frequently escape detection. If the
transparency is perfect the recognition of the detachment depends
solely on the appearance of the vessels. More commonly the
transparency, although sufficient to allow of a good choroidal
reflex being seen, is not absolute. In these circumstances the
summits of the folds into which the retina is thrown reflect the
light and appear white, as in Plate XL VI., Fig. 101.

A rent can be sometimes observed in the retina. Much more
frequently it is either too peripheral to be seen, or is hidden by
some folds of retina.

Detachment occurs first at the periphery, and tends to spread

TUMOUR AND DETACHMENT.

217

towards the centre, especially, if it is situated above. When very
extensive it obstructs the view of the remainder of the fundus.
Occasionally, the detachment reaches to the macula, if the retina
remains attached here, as it usually does for a time, the fovea is
seen of its natural colour lying at the bottom of a depression.
In a case under my care the outline of the macula was marked
out by a grey line which, from the parallactic movement, evidently
lay on a level anterior to the macula. It is probable that in this
instance the retina had torn away from the macula, and that the
grey line represented its free edge.

Except in recent cases, there are usually several distinct folds
of detached retina lying at different levels.

When the retina is pushed forwards by a solid growth, as a
choroidal sarcoma, the displaced portion is sometimes smooth and
dome-shaped, and it may present a dark slate colour owing to the
pigmented tumour showing through it. In some cases the vessels
on the surface of the latter can be made out. In these cases
there is usually also an ordinary detachment at a distance from
the tumour, which does not differ from one produced by other
causes.

The vitreous is seldom completely clear in detachment of the
retina. It usually contains some floating opacities, and not
unfrequently it is sufficiently turbid to render the diagnosis
difficult or impossible. In the great majority of cases the lens
eventually becomes opaque, and in time assumes that uniform
yellowish-white appearance which has already been described as
characteristic of a blind eye. In such cases the tension is
generally subnormal.

Detachment always shows a decided tendency to increase,
and, although in the later stages the media are too opaque for
ophthalmoscopic examination, total detachment can frequently
be seen in a section of an eye after enucleation. In such specimens
the retina comes forwards from the optic nerve entrance in the
form of a hollow tube, which anteriorly spreads out to reach the
28

218

DETACHMENT OF THE RETINA.

ora serrata, the whole structure somewhat resembling a con-
volvulus flower. In the centre, running from the disc to the
back of the lens, there can often be seen a fibrous cord, which is
the sole remnant of the degenerated vitreous. Occasionally, cysts
can be seen in the substance of the retina in these old
detachments.

(Edema of the retina can hardly be mistaken for detachment if
the media are sufficiently clear to permit a thorough examination.
The appearance is much softer and more uniform, the vessels are
not wavy, and the retina is not thrown into folds (see Plate XXV.,
Fig. 58). A mistake might more easily be made in the case of
fixed membranous opacities in the vitreous, which, when extensive,
have been named retinitis proliferans. Here, however, the opacity
is more glistening, and the membrane is tightly stretched instead
of being wavy. Detachment of the retina is not unfrequently
associated with this affection.

Commotio Retinae.

Blows on the eye from a blunt body are sometimes rapidly
followed by a diffuse cloudiness of the retina — a condition which
has received the name commotio retinae.

The injury is usually severe, and is followed by impairment of
vision, episcleral injection, and a spasmodic contraction of the
pupil, which only a very free employment of atropine will over-
come. For these reasons the fundus has often not been examined
sufficiently soon after the accident for the changes, which are
somewhat evanescent, to be discovered.

If the fundus be examined in about an hour after the injury,
certain parts of it will be seen occupied by a smooth greyish -white
cloudiness, like that which is present in embolism (Plate XXV., Fig.
58, and Plate XLI., Fig. 93). At first the cloud is thin in places,
thus allowing the fundus-reflex to be visible through it, but in a
short time the denser portions increase, and the whole surface may

COMMOTIO RETINAL.

219

become white. The retinal changes reach their height in from
twenty-four to thirty-six hours, there may then be a greyish-
white area ten or twelve times the diameter of the disc, shading
off gradually at its margins into healthy retina. The vessels
usually pass over it unaltered, but they may appear to be slightly
diminished.

The process then begins to subside. The opacity becomes less
dense, so that the fundus-reflex is again visible, and it diminishes
in area, so that in three days (sometimes even in two) from
the commencement of the subsidence, the fundus may have
regained its normal appearance.

Berlin 1 was the first to give a connected account of commotio
retinae, and no better description of the symptoms has since been
published. The above remarks are largely derived from his
original paper.

It will be noted that while the condition resembles detach-
ment in following a blow, and in presenting a white surface in
place of the normal red reflex, yet it differs from it in that there
is neither any alteration in the level of the retina, nor any
indication of its being thrown into folds.

1 Zehender, Klin. Monatsbl f. Auc/enh., Stuttgart, 1873, p. 44.

PLATE I.

PHYSIOLOGICAL CUPPING OP OPTIC DISC.

Fig. 1. — Physiological Cup.

Alice W., 18. LE. Draiving made in 1888. — A healthy girl, of moderately fair com-
plexion. Y. — 1 "5 =

Description. — Margin of OD. pigmented. A large physiological cup, having a diameter
slightly greater than half that of the OD. On its floor the mottling produced by the
lamina cribrosa is well seen. The cup is deepest on its nasal side, where the difference in
refraction between floor and edge was 3 D.

In 1894 the condition was unchanged.

Fig. 2. — Physiological Cup. Connective Tissue Ping.

Arthur P., 12. LE. Drawing made February 1890. — Low hypermetropia. Y. normal.
Description.- — The centre of the OD. presents a cup of circular outline. The floor of
this is shown out of focus ; when in focus it could he seen to be stippled, as in Fig. 1. The
circumference of the disc presents a pale soft-looking band— the connective tissue ring.

Fig. 3. — Physiological Cup. Oval Disc. Striation of Upper
and Lower Borders.

Minnie W., 12. IjE. Drawing made November 1889. — Complexion moderately dark.
Hair dark brown. Slight hypermetropia, no astigmatism.

Description. — Physiological cup steep towards centre of OD., shelving gradually to-
wards temporal border. Slight blurring of upper and lower borders of disc by a greyish
film, presenting evidence of striation. Margin of OD. pigmented. Downwards and out-
wards an irregularity of margin, as if the fundus had encroached on the disc.

Plate I

Fig. l. L.E

Fig 2 L.E

Fig 3. L.E

PLATE II.

RETINAL REFLEX.

Fig. 4. — Moderately Dark Fundus. Striation of Disc Margin.

Dark Macula.

Edward V., 7. LE. Drawing made, November 1889. — Moderately dark complexion.
Hypermetropia.

Description. — Fundus slightly darker than preceding figures. Striation of disc margin
well marked, and extending a good way from disc, especially above.

Macula seen as an area of darker colour than the fundus.

Fig. 5.— Very Dark Fundus. Retinal Reflex. Oval Disc.

Fovea Centralis Conspicuous.

Florence P., 11. LE. Drawing made 1889. — Dark olive complexion. Irides dark
brown. Hair almost black. Hypermetropia, 8 D. No astigmatism. Corrected Y. f.

Description. — Fundus has a dirty reddish-brown colour. Over the greater part of
fundus is a grey gauzy film, showing striation. This is most marked near the disc. Disc
oval, vertical diameter being to transverse as 1'7 to 1. The macula is seen as a dark-red
area, the retinal reflex being absent here. In its centre the fovea centralis seen as a round
white spot.

The “ watered-silk ” appearance of the retina was well marked, but has been purposely
omitted from the drawing.

Fig. 6. — Dark Fundus. Retinal Striation Limited to Disc-Margin.

Disc of Rich Red Colour.

Boy, 10. RE. Drawing made in 1891. (Lent by Mr. Hartridge.) — Complexion dark.
Irides dark brown. Hair black.

Description. — Fundus of dull red, intermediate in colour between Figs. 4 and 5. Disc
surrounded by a striated halo. Colour of disc a warm red. Macula dark. Fovea not visible.
The distribution of the vessels is typically normal.

Plate ii

Fig .4-.LE

Fig. 5. R.E

F i g . 6 . L. E

PLATE III.

FUNDI, SHOWING CHOEOIDAL VESSELS.

Fig. 7. — Light Fundus. Choroidal Vessels with Light Interspaces.

Lena L., 8. EE. Drawing made March 1892. — Very fair complexion, light hair, blue
irides. Slight hypermetropia. V. = f.

Description. — Over the greater part of the fundus a large number of choroidal vessels
are visible. The spaces between them are reddish white. In the central region no choroidal
vessels are visible, and the fundus is darker. The macula is seen as an area having a
slightly darker colour than the surrounding fundus.

The disc margin has a soft appearance. White lines accompany the inferior temporal
artery on the disc.

Fig. 8.— Dark Fundus. Choroidal Vessels with Dark Interspaces.

Retinal Reflex.

Edith S., 7. EE. Drawing made in 1888. — A brunette. Irides dark brown.

Description. — Over the part of the fundus that surrounds the disc the choroidal vessels
are visible. The spaces between them have a brownish-black colour, an appearance some-
times called “ Chorioide tigree.” Over the same area can be seen fine lines radiating from
the disc. These, like those in Fig. 5, are due to light reflected from the retina. The
macula is seen but faintly, and there are indistinct lines radiating from its centre. Near
the macula are several minute white dots. With the ophthalmoscope these were seen best
with a feeble illumination — “Gunn’s dots.”

■

Plate ill

Fig. 8 R E

F10.7.R E

PLATE IV.

CONGENITAL CRESCENT OE OPTIC DISC.

Figs. 9 and 10.— Congenital Crescents. “Gunn’s Dots.”

Fig. 9. — Alice H., 11. RE. Drawings made 1888.

Y. (under atropine) = T6g c. + L5 sp. 0 + 075 cyl. | = £.

Description. — Occupying the lower tenth of the disc a pale crescent, its surface
slightly stippled. Its arms pass round the disc, becoming narrower and continuous with
the connective tissue ring.

The border of the disc is pigmented, and there are lines of pigment on the fundus,
concentric with the temporal border of the disc.

The macula is visible as a dark red area. On, and near, it are several small yellowish

dots.

Fig. 10. — Represents the LE. of the same patient.

Y. (under atropine) = 36g c. + 3-0 sp. O + 0‘50 cyl. | =f.

Description. — Occupying a little less than the lower fourth of the vertical diameter
of the disc, a pale crescent, stippled with grey. Margin of disc less pigmented than RE.
Surrounding the disc a light yellowish halo — retinal reflex. Lower vein on the disc
crossed by a few delicate connective tissue fibres. Macula as in RE., but fewer dots. The
dots were only visible in certain positions of the ophthalmoscopic mirror; when seen they
were always in the same position.

Plate iv

Fig. 9. r e

Fig. 10. L.E

PLATE V.

VARIATIONS OF DISC MARGIN.

Fig. 11.— Pigment on Disc. Connective Tissue on Disc.

Ernest W., 6. RE. Drawing made in 1888. — V. (under atropine) + l'0o + 0\50 cyl. | = f.

Description. — The temporal border of the disc presents a considerable mass of black
pigment which encroaches upon the disc. The retinal vessels on the disc are crossed by
numerous fine bands of connective tissue. The upper and lower veins proceed an unusual
distance before giving off any branches.

Fig. 12. — Absence of Central Zone of Disc. Peculiar Colour.

Connective Tissue Ring.

Daisy S., 12. LE. Drawing made in 1889. — V. (under atropine) - 6'0 - 1‘50 cyl. — = /V.

Description. — The disc is of a uniform dull red colour, as if the red were mixed with
grey. The vessels disappear into the centre of the disc gradually, as if they were dipping
into a semi-transparent substance. The colour of the disc extends right up to the point of
entry of the vessels. The disc is encircled by a white band of unequal width In the
greater part of its extent, it resembles the connective tissue ring as seen in Fig. 2, but on
the temporal border it is broader and whiter. Numerous choroidal vessels are visible, one
of unusually large size.

The patient was seen in 1894, and the conditions showed no appreciable change.

Fig. 13. — Physiological Cup. Narrow Crescent on Temporal Boruer.

Laura P., 14. RE. Drawing made December 1892.

Description. — A large physiological cup, deepest near the centre of the disc. It appears
to reach to the temporal border, gradually becoming more shallow. On the temporal border
of the disc is a narrow white crescent, more brilliantly white, and more sharply marked off
from the disc than is usual with a connective tissue ring.

Fig. 14. — Grey-Red Disc. Exaggerated Connective Tissue Ring.

Joseph P., 51. RE. Drawing made in 1888. — V. (under homatropine) + PoO = £ each eye.

Description. — The greater part of the disc is of a greyish colour, tinged with red.
Encircling this, and not very sharply marked off from it, is a white band, broadest on the
temporal border.

The other eye presented a similar condition, but the disc was redder, intermediate in
colour between that of this Fig. and that of the disc in Fig. 12.

• I .. 1 -«

■

Plate V

Fig 11 R.E

Fig. 12. R.E.

Fig. 13. R E

Fig. 14. R E

PLATE VI.

CONGENITAL CRESCENT OF OPTIC DISC.

Fig. 15. — Congenital Crescent. Cilio-Retinal Vessel.

Ernest E., 7. LE. Drawing made in 1888. — V. (under atropine) + 4-5 = £.

Description.— There is a large physiological cup. The uncupped part of the disc has a
peculiar plum colour. Below is a pale crescent, having a maximum width equal to one-fifth
of the vertical meridian of the whole disc. It extends further round the disc on the
temporal than on the nasal side, and is continuous with a narrow pale band which encircles
the disc. Surrounding the disc is a pale yellow halo.

At the lower and outer edge of the disc the^e emerges a large artery — cilio-retinal,
which almost immediately bifurcates, and is distributed to the lower temporal quadrant
of the retina.

Figs. 16 and 17. — Congenital Crescents, Large Physiological Cups.

Fig. 16. — Eliza C., 11. RE. Drawings made in 1888.

V. (under atropine) + 1 '0 O + 0\50 cyl. — = -£.

Description. — A large physiological cup, opening downwards and outwards. The un-
cupped portion of the disc is of crescentic shape, and of a dark dull red colour. The two
large -temporal veins curve boldly round the edge of this.

In the lower temporal margin of . the disc a crescent, measuring at its widest part, a
sixth of the total diameter of the disc. Well marked pigmentation of disc margin.

Fig. 17. — Represents the LE. of the same patient. V. (under atropine) as RE.

Description. — Very similar to Fig. 16, but the crescent is narrower; the colour of the
disc not as dark.

. •

‘ • . Plate vi

Fig. 15. L.E

PLATE VII.

CONGENITAL CEESCENT OF OPTIC DISC.

Figs. 18 and 19. — Congenital Crescents. Tortuous Veins.

Fig. 18. — Alice B., 7. Drawings made in 1888. — RE. correcting lenses, as found by
shadow-test, + P500-j-4'0 cyl. | .

Description. — At the lower part of the disc is a white crescent, measuring at its
widest part about a sixth of the total vertical diameter of the disc. The remainder of the
disc has a peculiar dull-red colour. There is no physiological cnp.

The superior nasal vein is unusually tortuous.

Above and below the disc the choroidal vessels are visible.

Fig. 19. — LE. of the same patient.

Kefraction as in RE.

Description.— AX, lower part of disc a white crescent, having at its widest part a
diameter equal to a fourth of the total disc diameter.

Several of the retinal veins run a very tortuous course. Above and below the
disc the choroidal vessels are visible.

Colour of the disc similar to RE., but darker.

Figs. 20 and 21. — Congenital “ Mottled ” Crescents.

Fig. 20. — John P., 15. RE. Drawings made in 1888. — V. + O'oOC -f- l'O cyl. | =XV

Description. — Physiological cup opening towards temporal border. The lower vessels
curve boldly round the margin of this. On the temporal side of the disc a crescent having
a mottled appearance. A cilio-retinal vessel emerges from its lower and outer border.
Choroidal vessels seen faintly round disc.

Fig. 21. — LE. of same patient. V. as RE.

Description. — Similar to Fig. 20, but crescent better marked. Choroidal vessels faintly
visible round the disc, with pigment between them. At the upper and outer part of the
disc-margin a rounded pale area with soft outline.

■

‘

■

Plate vii

PLATE VIII.

CONGENITAL CRESCENT. COLOBOMA OF DISC.

Fig. 22. — Congenital Crescent.

Florence G., 18. LE. Drawing made in 1888. — Y. - 5'0 cyl. = -J. BE. a small crescent
below the disc similar to Fig. 18. Y. - 7'5 - =f.

Description. — The disc consists of two parts. The upper, which is slightly the larger,
is of a dull red colour, and the vessels disappear into it gradually, as if passing into a semi-
transparent substance. The lower portion, which forms the crescent, is white, stippled
with grey.

In 1894 the condition was unchanged.

Fig. 23. — Congenital Crescent Above.

Alice R, 18. LE. Drawing made in 1890. — V. - 3-0 - l-50 cyl. — = TV
In BE. a similar crescent below Y. downwards and inwards. Y. - 0-50 - 2‘50^-20° = TV
Description.— The crescent is large, and somewhat pointed above. The remainder of
the disc is oval, and presents a physiological cup with a sharp lower edge, over which the
vessels curve abruptly.

Twto years later the myopia had increased 2 D., and the corrected V. in each eye was f.
There was no change in the appearance of the discs.

Fig. 24. — Congenital Abnormality of Disc (Partial Coloboma ?).

Joseph J., 48. BE. Drawing made November 1890. — Y. - 1’75 - L75 cyl.-~-~~20o = 4 partly.
The LE. presented a somewhat similar appearance. — V. - 3'0 - 3'5 — 0 f partly.

Description. — The whole disc area has about twice the normal diameter. Within this,
nearer to its upper than its lower border, is a circular area, a little smaller than the normal
disc, of dull reddish-grey colour, resembling the coloured portion of the disc in Fig. 22, but
less red. The circumferential portion consists of a broad band, wider below than above; this
is white stippled with grey, like the crescent in Fig. 22.

The upper veins curve over the boundary line between the white and red portions, as if
they were dipping into a cup. The other vessels disappear gradually into the red portion.

Subsequent History. — Seen November 1894 — no change.

Fig. 25. — Coloboma of Disc.

Robert P., 15. BE. Drawing made June 1890. Compound myopic astigmatism.
Corrected vision -j^-.

LE. Emmetropia. V. = f . In this eye a small congenital crescent down and in.

Description of BE. — The whole disc area has a diameter about twice that of a normal
disc. It is slightly irregular in shape, but is approximately circular. At the lower part, is
a crescent, measuring at its widest part about a fourth of the whole vertical diameter ; the
arms of this crescent embrace the remainder of the disc. The upper margin of the crescent is
sharply defined, and the lower vein curves over it, as if dipping into a cup. The remainder of
the disc consists of two parts which, however, are not sharply separated. The upper is the
colour of a normal disc, the lower, smaller, is similar in colour to 22. Into it some vessels
gradually sink.

Subsequent History. — Seen November 1893 — no change.

Plate viii

Fig. 22. L.E

Fig 23. L.E

Fig. 24. E.E

Fig. 25. R E

PLATE IX.

COLOBOMA OF FUNDUS.

Fig. 26. — Coloboma of Fundus.

Woman, 45. LE. Drawing made October 1888. (Lent by Mr. Hartridge.)

RE. presented nothing abnormal. V = £.

LE. Y. = Ar- Triangular defect in visual field above. A typical coloboma of the iris.

Description. — A large white area extending from half a disc diameter below the disc
downwards to beyond the limit of ophthalmoscopic examination. The margin is sharply
defined and pigmented in places. Above it looks like the sharp edge of a depression, an
effect which is increased by the manner in which the retinal vessels curve over.

The disc is oval ; its long diameter transverse. Above it is a crescent on which some
small vessels are visible.

Fig. 27. — Coloboma of Fundus.

Mrs. 0., about 40. RE. Drawing made March 1889.

LE. Y. = TU, Hm. = D5 D. External

fundus divide off a smaller portion above,
resemblance to the patch that existed in RE.

appearance normal. Below the disc a
circular patch of exposed sclerotic having
a diameter about twice that of the disc.

RE. coloboma of iris, Y. = A tri-
angular defect in upper part of field.
Typical coloboma of iris.

Description. — Extending downwards
from about two disc diameters below the
disc to beyond the limits of ophthalmo-
scopic examination, a white area of scleral
whiteness, widening towards the periphery,
its surface is stippled in places, and its
border pigmented. A transverse line of
pigment and a small tongue of normal
This portion bears in size and position a

Plate IX

Fig 26. L E

PLATE X.

CONGENITAL PIGMENT DOTS ON FUNDUS

Fig. 28.— Congenital Pigment Dots.

Jno. W., 5. LE. Drawing made in 1888. — The youngest of six living children. There
was no consanguinity of the parents. The other children presented no similar condition,
but two of them had a pigment spot on the disc, close to its temporal border.

The RE. presented nothing abnormal.

Description. — Groups of pigment dots scattered over the lower sector of the fundus.

Fig. 29. — Congenital Pigment Dots.

Sidney P.,13. LE. Drawing made in 1888. — The fifth of seven children. There was no
consanguinity of the parents. Four of the other children and the mother were examined,
and presented no similar appearance. V. (under atropine) each eye+l’75=£.

Patient stated, in answer to questions, that he saw worse at night than the other
boys in the school, but there was evidence of the correctness of this statement.

The RE. presented nothing abnormal.

Description. — In the upper part of the fundus several groups of pigment dots. The
groups are fewer than in Fig. 28, but the dots composing them are more numerous and
more closely aggregated.

The fundus is of the sombre-red type. Macula visible as a still darker area. Retinal
striation round disc well marked.

Subsequent History. — A year later these cases were unchanged.

Note. — Drawings of both these cases formed part of a paper read by Mr. Sydney Stephenson before the
Ophthalmological Society, and published in Vol. XI. of the Transactions. They are now published
by permission of Mr. Stephenson and of the Council of the Ophthalmological Society.

Plate x

Fig 28 XX

Fig. 29. R E

PLATE XI.

PUNCTATE CONDITIONS OF FUNDUS.

Fig. 30. — Physiological Dots in Macular Region. (“Gunn’s Dots.”)

George P., 11. RE. Drawing made in 1888.

There were corneal nebulae in both eyes.

Y. (under atropine) RE. + U25 = f.

LE. + 175 = f.

The macular halo, and the “ watered-silk ” appearance of the whole retina were con-
spicuous, but have been purposely omitted from the figure.

Description. — Fundus of the moderate light type. Macula seen as a dark area. On
this, numerous yellowish minute dots; a little lower down, two small groups of similar dots.
These dots could only be seen in certain positions of the ophthalmoscopic mirror, but when
seen they were always in the same position. In the drawing they are necessarily too
conspicuous. For similar dots see Figs. 9 and 10. Nearer the disc are two pairs of dots
which are somewhat larger, and are possibly of a different nature.

Large physiological cup, the “ intermediate zone,” being reduced to a crescent. The
distribution of the vessels on the retina is typically normal.

Fig. 31. — Diffuse Punctated Condition of Retina.

Mrs. P., 43. RE. Drawing made in November 1888. — The patient had been seen in 1884,
and the ophthalmoscopic appearance had not appreciably changed. Y. RE. + 2-5 = /W.
LE. + 2 '5 = f, slight concentric contraction of right VF, and considerable contraction of
left. The ophthalmoscopic appearances were similar in the two eyes.

Description. — The disc is normal, and presents a complete connective tissue ring. The
whole fundus is closely sprinkled with small pale dots. Towards the macula the dots are
larger and fewer, they are absent from the central part of this region. Towards the peri-
phery of the fundus, the dots are packed less closely, but are still numerous. The
largest have a diameter equal to that of a primary branch of the retinal artery, the smallest
are so minute as to be barely visible. The great majority are of a nearly uniform size
intermediate between these extremes. The dots are of a dull yellowish-white colour, are
devoid of brilliancy, and have a soft appearance. They lie entirely beneath the retinal vessels.

No pigment deposits were seen anywhere, except the ordinary pigment line near
the disc.

The patient was seen again at intervals till 1896, and no appreciable change was
observed in the appearances.

■' ■

■

Plate XI

Fig. 30.EE

Fig. 31 R E.

PLATE XII.

CONNECTIVE TISSUE ON DISC AND OPAQUE NERVE FIBRES.

Fig. 32.— Connective Tissue on Disc.

Henry A., 13. RE. Drawing made in 1888.

V. under atropine iL6,. + 3-0ZtO + l-0 cyl. — =f.

LE. + 3' Oo + 1'5 cyl. — =f (3 letters).

The condition in the LE. was similar, but less marked.

Description. — Whole fundus faintly stippled with pigment. To the nasal side of the
centre of the disc a broad vertical white band, lying in front of and concealing the vessels.
From this numerous fine white threads pass over the upper part of the disc, and a few over
its inner part.

Fig. 33. — Connective Tissue on Disc.

Margaret B., 10. LE. Drawing made in 1888.

V. under atropine RE. + 7'0D = f (2 letters).

LE. + 7’0 = f (3 letters).

Description. — Fundus mottled with fine pigment. Choroidal vessels seen faintly. A
nearly vertical white band in centre of disc. Offshoots from this accompany the upper
and lower vessels, and two others pass outwards. Retinal striation seen on upper part of
disc.

Fig. 34. — Opaque Nerve Fibres.

Emily A., child. RE. Drawing made in 1888.

Description. — Fundus of the moderately dark type. Projecting from the upper part of
the disc two broad brilliantly white, finely fibrillated processes. They conceal the upper
border of the disc, and lie beneath the retinal vessels. The fibrillar nature of the patches
is best seen at their peripheral extremities, where the component fibres separate from each
other.

Fig. 35. — Opaque Nerve Fibres.

Frederick H., 13. LE. Drawing made in 1888.

Vision each eye = f.

Description. — Two masses of brilliant white fibres proceeding from the lower margin of
disc. Several of the fibres pass in front of the vessels. The fibres appear to form a thin
layer, the fundus being visible between them in places.

■

Plate xii

Fig 32.EE

Fig. 33 LE

Fig. 34. R E

Fig. 35. L.E

PLATE XIII.

OPAQUE NERYE FIBRES.

Figs. 36 and 37. — Opaque Nerve Fibres.

lig. 36. — John F., 12. HE. Drawings made in 1888.

Y. +4 OD. Ol'O cyl. | = £.

Description. — Fundus of the moderately dark type. A dense, hard-looking mass of
white fibres surrounding the disc, and concealing its upper and inner part. The remainder
of the disc has a peculiar plum colour. Some of the vessels are completely hidden in
places ; others are seen faintly through the fibres.

Fig. 37. — LE. of the same patient. Y. + 5 OD. Ol’O. cyl. | =

Description. — The distribution of the fibres differs somewhat from that seen in Fig.
36, and less of the disc is covered ; in other respects the two eyes are similar.

Plate xiii.

PLATE XIV.

OPAQUE NERVE FIBRES.

Fig. 38. — Opaque Nerve Fibres.

Rachel V., about 12. LE. Drawing made in 1888.

Description. — Above the disc two masses of opaque nerve fibres. That on the temporal
side is separated from the disc by a narrow strip of normal fundus.

Fig. 39. — Opaque Nerve Fibres.

Eliza L)., 40. RE. Drawing made in Januarg 1890.

V. (under homatropine) 4-1 '5 + 1 "50 cyl. — = f. — The visual field was taken carefully,
and the area of the blind spot found to be perceptibly increased.

Description. — A large white fibrillated mass covering nearly two-thirds of the disc,
and extending about three disc diameters on to the fundus. The vessels, where covered, are
for the most part entirely hidden.

Plate xiv

Fig 39 .

PLATE XV.

CHOROIDITIS.

Fig. 40. — Choroiditis. Early Stage.

Essie W., 24. BE. Drawing made October 1889. — A healthy looking girl. No evidence of
syphilis, inherited or acquired. Both parents living and in good health. An elder brother
sutlers from tubercular disease of the hip. Family and personal history, in other respects,
unimportant.

The patient was seen in March 1889 for dimness of LE. due to “ keratitis punctata.”
The dots were minute ; there was no circumcorneal injection. Pupil active, no adhesions.
A few weeks later the BE. became affected in a similar manner. The patient was treated
with mercury. The corneie cleared after a few weeks, and the condition of the fundus,
depicted in Fig. 40, was then discovered. The LE. presented a similar appearance. The
Y. at this time was BE. + 0'50 = LE. - 050 = f, .

Description. — Disc normal. On the temporal side, beyond the connective tissue ring, a
mottled crescent, on which several choroidal vessels are visible. On the nasal border a
brush of connective tissue or of opaque nerve fibres. Between the disc and macula, numerous
irregular pale areas mottled with fine pigment. Above a disc of pigment, a pigment ring
enclosing healthy fundus, and another enclosing an atrophic area. The periphery of the
fundus was normal.

Subsequent History. — The case was seen at intervals till April 1894. During this
period there were, at least, five attacks of “ keratitis punctata ” in each eye ; sometimes one
eye and sometimes the other being affected. It is probable that there were other slighter
attacks or relapses. V. varied only with the condition of the cornea. No appreciable
change took place in either fundus.

Fig. 41. — Choroiditis. Advanced.

Miss L., 20. LE. Dravjing made March 1889. — Physiognomy typical of inherited syphilis.
Patient very deaf. Both cornea.1 presented central cloudiness, the remains of former keratitis.
She is the youngest of twelve children, eight of whom died in infancy, and one later of
consumption. One of the survivors, a sister, who was the eldest of the family, was seen,
and presented no signs of inherited syphilis. The other survivor, a brother, was not seen, and
no reliable account of his condition was obtained. Patient stated that her sight has always
been defective ; eight years ago both eyes became inflamed, and continued so about a year.

Y. BE. = t6¥ ; LE. counts fingers. The condition of the fundus of BE. was not noted.

Description. — Over nearly the whole fundus are numerous circular patches of choroidal
atrophy. The larger round or oval, the smaller more irregular in shape. Most of these are
partially surrounded by pigment which also tends to form a network with irregular meshes,
inclining to a circular shape ; some of this pigment lies in front of the retinal vessels.
Towards the disc the choroidal changes cease rather abruptly ; a space of about two disc
diameters on the temporal side of the disc being almost normal.

:Vh

■

Plate xv.

Fig 40, R E

Fig. 41, L.E.

PLATE XVI.

CHOROIDITIS.

Fig. 42. — Chokoiditis. Advanced.

Harriet E., 24. LE. Drawing made February 1890. — The teeth were typical of inherited
syphilis ; in other respects the patient’s physiognomy presented nothing characteristic.
Patient is the fourth of ten children, two of whom died at birth, and two during infancy.
No further details obtainable. V. RE . = TV

LE. There was a posterior polar cataract, and there were a few floating opacities in
the vitreous. V. hand movements.

Description. — Numerous round and oval areas of choroidal atrophy. They vary in
size, the larger having a diameter twice that of the disc. In all, the sclerotic is completely
exposed, although many are crossed by a few choroidal vessels. Above the disc a
large area evidently formed by the coalescence of smaller ones.

Near the macula is a group of five small circular areas of exposed sclerotic. Some of
the patches are surrounded by pigment, but in most situations the pigment seems to
be deposited without reference to the atrophic areas.

Plate xvi

PLATE XVII.

CHOROIDITIS. Advanced.

Fig. 43. — Choroiditis. Secondary Pigmentation of the Retina.

Mary A., 60. RE. Drawing made in 1890. — Said to have had good health till her marriage
at the age of twenty. Fifteen months later she was delivered of her first child, craniotomy,
or some analogous operation, being performed. A few months later nearly all her hair came
off. She next had a miscarriage. Then, eighteen months after her first confinement, a child,
which was said to have been healthy, hut it died of “ fever ” at the age of twelve. Then
followed two miscarriages, and then two children in succession, each of whom died at about
thirteen months from “ fits.” Her sight began to fail a few months after her first confine-
ment, and has steadily deteriorated since. Y. is now RE. - 2 D = T\] LE. fingers. But at
night her sight is so much worse that she has to be led.

The ophthalmoscopic appearances in the two eyes were similar.

Description. — An immense area of exposed sclerotic surrounding the disc, except on
its temporal side. Beyond this large oval areas, almost in contact with each other, and a
few similar isolated patches. The macula is free from these, but presents a good deal of
pigment deposit. There are large masses of pigment in several situations.

Plate xvil

PLATE XVIII.

DISSEMINATED CHOROIDITIS.

Eig. 44. — Disseminated Choroiditis with Conspicuous Pigmentation.

Amy D., 29. IiE. Drawing made July 1890.

She enjoyed good health till her marriage in 1878. About a month later she
noticed a vaginal discharge, and two weeks after this a rash appeared all over the body,
which persisted for a year, and left permanent scars. In July 1879 the vision of HE. began
to fail. She believes that the LE. was always defective.

She had no miscarriages. Her first child was born in April 1881. The child, when
seen in 1893, had typical syphilitic teeth, and was suffering from choroiditis, with pig-
mentation of the retina, and recent iritis. Two other children were born in 1883 and 1885
respectively. One died of pleurisy, the other is said to be healthy, but has not been seen.

The fundus of RE. was first examined in 1885 ; at the date of the drawing it had not
appreciably changed. The LE. presented similar changes, but in addition there was a
connective tissue formation in the macular region.

Description. — On the temporal side numerous circular areas of partial atrophy of the
choroid. The majority are circular or oval ; some are surrounded by a border of pigment.
On the nasal side there are areas of similar size, so closely aggregated as to be almost in
contact. The majority of these are almost completely covered by pigment, those which are
only bordered by pigment show less atrophy than those on the temporal side.

Subsequent History. — The patient was seen at intervals till 1896, and no appreciable
change occurred.

Jr1

Plate XVIII

Fig. 44. B. E

PLATE XIX.

PIGMENTATION OF RETINA SECONDARY TO CHOROIDITIS.

Fig. 45. — Pigmentation of Retina from Choroiditis.

Henry S., 45. RE. Drawing made February 1889. — Twenty years ago lie noticed “ black
spots ” before the RE. ; the vision failed gradually soon afterwards, and has been defective
ever since. There was no history of acquired syphilis, nor were there any signs of an
inherited taint.

RE. V. = hand movements, and that only on the outer part of the field.

LE. Y. = f. Ophthalmoscopic appearance normal.

Description. — Disc rather pale and dull -looking. Connective tissue ring well marked.
The superior temporal artery is of fair size, but its branches are small. In the lower part of
the retina only one artery is visible, and this is a cilio-retinal vessel. The choroidal vessels
are seen as pale streaks. Towards the periphery numerous pigment rings, enclosing fundus of
normal colour. Above the disc are some circular areas of pigment like those in Fig. 44.
In some situations the pigment forms a network — the meshes tending to assume a
circular form.

Plate XIX

Fig. 45.EI.

PLATE XX.

DISSEMINATED CHOROIDITIS.

Fig. 46. — Disseminated Choroiditis. Stage of Exudation.

William S., 39. BE. Drawing made October 1888. — In 1883 he had a chancre, followed
by sore throat and rash ; he was under treatment for six months and considered himself
to be cured. In March 1887 his sight became defective, especially at dusk. In July
1887, V. BE. = tt\-, LE. = jV. Numerous very fine opacities in the vitreous. The fundus

of BE. as depicted. The LE. presented a similar, but less advanced, condition. At the

date of the drawing, Y. BE. = de ; LE. = TfV.

Description. — Margin of disc indistinct. Scattered over the fundus numerous soft-
looking pale areas of roundish shape, the majority varying in diameter from { to }

of the diameter of the disc. Besides these there are very numerous small pale dots

crowded together over the whole fundus.

Note.— This patient was originally under the care of Mr. Hartridge, who published the case, with a chromo-
lithograph, Trans. Oplitli. Soc., U. Kingdom, London, Vol. IX., 125. This Figure is reproduced from
the original drawing by permission of Mr. Hartridge, and of the Council of the Ophthalmological
Society.

Fig. 47. — Disseminated Choroiditis. Stage of Atrophy.

Drawing made March 1891. — It represents a later condition of the same fundus
as Fig. 46. V. BE. = hand movements only. LE. =4' 5 Snellen. The fundus of IjE.
presented a similar appearance.

Description. — The smaller pale dots have disappeared. The choroidal vessels are
more visible. In place of the soft-looking pale areas there are sharply defined larger
areas of exposed sclerotic, which have retained a round or oval shape. Some of these
have an incomplete pigment border, and there are other incomplete pigment rings.
The margin of the disc is well defined.

■

Plate

PLATE XXI.

CHOROIDITIS. Atrophic Stage.

Fig. 48. — Areas of Choroidal Atrophy without Pigmentation.

William L., 70. RE. Drawing made in 1888. — Patient has always been in good health.
He is robust in appearance and looks younger than his years. No history of syphilis.

V. RE. y6g- + 1-5 = XV Ophthalmoscopic appearance as depicted.

LE. Ts\+ 1\5 = ■§•. A few patches of choroidal atrophy.

Description. — Fundus of the dull red type, like that shown in Fig. 15. Choroidal
vessels faintly seen.

The inferior temporal vein runs a very tortuous course near the disc, and there is a
twist in the superior nasal vein. Several round and oval areas of choroidal atrophy,
crossed by vessels. None of the areas have a complete pigment border, and the majority
show no pigment.

PLATE XXII.

CHOROIDITIS AT MACULAR REGION.

Fig. 49. — Superficial Choroiditis at Macula.

Sarah B., 49. RE. Drawing made October 1890. — Attended for failure of V. due to
“ keratitis punctata.” Y. RE. + L25 = yY. LE. + l-0 = She was at this time under treat-
ment for a syphilitic rash. The cornea cleared, and Y. of LE. improved to f , but that of RE.
became reduced to counting of fingers, and this only in the lower and outer part of the
field. The fundus of the LE. was normal.

Description. — The central region for a space of about 3 del occupied by round, pale,
flat-looking areas, closely aggregated. The largest have a diameter equal to about ^ that of
the disc, but at the circumference of the affected area there are much smaller spots.
Between the central patches, the fundus is dark. There is no deposit of pigment anywhere.

Subsequent History. — In January 1892 the pale areas on the fundus had not appreciably
changed in size or number, but there were distinct indications of choroidal vessels crossing
the larger ones. In front of the disc (2 dd) two small red spots of irregular shape, con-
nected by a gauzy material, which was difficult to see owing to its transparency. No
vessel could be seen to have any connection with these spots.

December 1893. — The two red spots described above, replaced by a distinct vascular
loop, formed by a single vein projecting from the inner part of the disc. The summit of the
loop visible with 4 D. Some of the larger pale spots at the lower part of the affected area
have become confluent.

Fig. 50. — Choroiditis at Macula.

Ann G. LjE. Drawing made October 1890. — Complained of recent failure of vision.
General health good. No history of syphilis. Y. each eye + 2-25 = T6s-.

The ophthalmoscopic appearances in the two eyes were similar.

Description. — Disc normal ; well marked connective tissue ring. The macular region,
for the space of about a disc and a half diameter, occupied by small roundish spots, a
few of the larger showing a scleral whiteness, and one of these is crossed by a choroidal
vessel. Most of the spots are pale and soft-looking. There is some pigment round the
whiter spots.

Fig. 51. — Choroiditis at Macula. Old.

Sophia E., 24. LE. Defect only discovered recently. V. = fingers. RE. Normal.

Description. — In macular region an oval patch of choroidal atrophy, crossed by a few
choroidal vessels. Surrounding it is a complete ring of pigment, and beyond it a narrow
band of pale fundus. The exposed sclerotic lay on a much deeper level than the adjacent
fundus.

Fig. 52. — Choroiditis at Macula. Old.

Kathleen F., 23. LE. Drawing made in 1889. — Defect recently discovered. V. = /ff.
RE. Normal.

Description. — An oval area of completely exposed sclerotic, crossed by choroidal vessels.
Surrounding this a broad belt of pale fundus, partly covered by pigment. Above and below
the pigment is more abundant, and through circular openings in it sclerotic is exposed.

Plate XXII

Fig 49 .R E

Fig 50 LI

Fig. 51. L Z

Fig. 52. L.Z

PLATE XXIII.

(Drawn by the Indirect Method.)

HIGH MYOPIA.

Fig. 53. — Myopic Crescent Stationary.

Alice D., 15. RE. inverted. Drawing made November 1888. — Moderately fair com-
plexion. Y. -14 _Z> = T6-g-.

Description. — Disc oval, with long diameter vertical. On its temporal side a crescentic
area of exposed sclerotic, having a regular, sharply-defined border. Choroidal vessels
visible over whole fundus.

Fig. 54. — Progressive Myopia.

Mary S., 42. RE. inverted. Drawing made January 1889. — Said to have been only
moderately short-sighted till ten years ago, and to have been gradually getting worse since.
In LE. numerous opacities in vitreous, extensive choroidal atrophy, Y. = 03 Snellen at
2 inches. Distant V. not improved to -g^-.

RE. peripheral strife in lens. V. not noted.

Description. — Disc oval, of a peculiar purplish colour. On temporal side of disc a
crescent of exposed sclerotic. This is connected with a large irregular area of exposed
sclerotic in the macular region. The central part of the latter shows some remains
of choroidal tissue and some pigment deposit. Partial atrophy of the choroid has taken
place immediately adjacent to the larger area.

Fig. 55. — Choroiditis and High Myopia.

Charles W., 38. RE. inverted. Drawing made in 1892. — Always short-sighted. Stated
that ten years ago he could read small print at about ten inches. In 1890 he attended the
Eoyal London Ophthalmic Hospital, and his V. was noted as ^ , and 2'0 Snellen at 6
inches in each eye. At date of drawing V. was DO Snellen at 4 inches, and the Myopia
was about 10 D. The LE. was similar.

Description. — On the lower and outer side of the disc an area of choroidal atrophy
approximately crescentic, but irregular, in shape. Scattered over the fundus numerous
rounded and irregular atrophic areas. The surface of many of these is speckled with
pigment, but none have a pigment border. Similar speckling with pigment is seen in
other parts of the fundus where there is no atrophy. The choroidal vessels are every-
where visible.

■

* 'M III

INDIRECT METHOD

Plate XXIII

Fig. 53. R E

(Inverted).

Fig 54.R.E

(Inverted).

Fig. 55. R E

(Inverted).

PLATE XXIV.

SENILE CHOROIDITIS AND POST-NEURITIC ATROPHY.

Fig. 56. — Senile Choroiditis.

Jabez C., 83. LE. Drawing made March 1892. — Has a typical senile aspect ; has always
enjoyed good health. Vision began to fail gradually two or three years ago, and became
steadily worse till six months ago, since which lie thinks that it has remained stationary.
V. in each eye At- The ophthalmoscopic appearance is similar in both eyes.

Description. — Disc of rather dark colour. Surrounding it a wide belt of choroidal
atrophy, which is complete, with the exception of some large vessels which remain. Beyond
the atrophic belt on the temporal side is an irregular area of partial choroidal atrophy. The
choroidal vessels are everywhere visible, and some of the spaces between them are pigmented.

Fig. 57. — Post-Neuritic Atrophy. Cicatricial Changes at Macula.

Choroidal Atrophy.

Margaret R., 27. RE. Drawing made December 1892. — V. RE. no p.l. ; LE. p.l. only. —
Five years ago was seized with headache and occasional vomiting. After two months these
symptoms subsided, and at the same time V. failed rapidly, reaching its present condition
in three months. The headache and vomiting have not recurred.

Description. — Disc greyish white, not mottled. Physiological cup visible. Surrounding
the disc a pale band of irregular width, continuous below with a broad pale area, while
above two processes shoot out from it. The larger of these forms a white band, with almost
parallel sides, but widens out fan-wise above. The whole fundus is sprinkled with fine
pigment dots.

At the macula an irregular star-like patch of pale colour, from which processes diverge
in all directions.

■

Plate xxiv.

Fig. 56. L.E

Fig. 57. R E

PLATE XXV.

RETINAL (EDEMA AND MEMBRANOUS FORMATION IN RETINA.

Fig. 58. — Choroiditis. (Edema of Retina.

Thomas W., 45. LE. Drawing made September 1889. — EE. normal in all respects.
LE. V. fingers only, date of failure of V. not stated. No history of syphilis was elicited.
Has suffered from stricture of the urethra.

Description. — A few circular areas of complete choroidal atrophy and numerous imperfect
pigment rings. Margin of optic disc slightly blurred especially downwards and outwards,
where it merges into a grey soft looking area, which extends for a distance of three disc
diameters on to the fundus. This shades off very gradually into the adjacent fundus.
Near its nasal border is a linear haemorrhage. Surrounding the macula, except on the
side next to the patch of retinal oedema, a series of short white lines directed as if radiating
from the centre of the macula.

Fig. 59. — Choroiditis. Membranous Formation in Retina.

Emily H., 24, married. LE. Drawing made October 1890. — The notes of this case are
incomplete, and the patient could not be traced. V. IlE. = LE. =

Description. — A few circular and oval areas of almost complete choroidal atrophy, and
some pale areas of similar size and shape.

In the central region, an irregular mass of glistening white tissue, in it are numerous
oval openings with sharply cut edges, and through these the fundus is seen as if on a deeper
level. The white tissue lies entirely beneath the retinal vessels.

Plate xxv

Fig. 58. L.E

Fig. 59. L.E

PLATE XXVI.

CHOROIDO-RETINAL SCLEROSIS.

Fig. 60. — Choroido-Retinal Sclerosis, or Diffuse Choroido-Eetinitis.

Edward S., 55. BE. Drawing made June 1889. — He enlisted at the age of 21, served
ten years in India, and left the service at the age of 37. Always had good health. No
history of syphilis was elicited.

Noticed no defect of vision till about a year after his discharge, when he experienced
some difficulty in seeing at dusk. This gradu-
ally increased, until he had to be led about after
sunset.

Y. BE. T6g- — 0'50 = yL- letters. LE. = hand
reflex only. The field of BE. showed great
concentric contraction. (See Chart.)

The field of the LE. could not be taken.

He is quite unable to walk alone after
dark, either out of doors, or in a room fairly
well lighted with gas.

The ophthalmoscopic appearances d. were
similar in the two eyes.

Description. — Disc rather dark, surrounded
by a pale halo. Retinal arteries very small,
except the superior temporal, which is only
slightly diminished. The light-reflex is absent from them.

Over the whole fundus an immense number of choroidal vessels are visible. Some
have the normal red colour, others are bounded by white lines, while others, again, are com-
pletely white. This is especially the case near the disc. The spaces between the vessels
are light chocolate-brown, except in a few places, where small red patches remain. At the
macula no choroidal vessels are visible. There are isolated superficial deposits of pigment
in several situations.

Plate xxvr

Pig. 60 R.E

PLATE XXVII.

CHOROIDO-RETINAL SCLEROSIS.

Fig. 61. — Choroido-Retinal Sclerosis or Diffuse Choroido-Retinitis.

Alfred R., 51. RE. Drawing made July 1890. — A gardener, has always lived in the
country. No history of syphilis or of malaria could be obtained. Patient looks in perfect
health. Has had no serious illness. Has been married twice. Two children, now grown-up,
by his first, and two by his second wife — all said to be healthy. His parents were not
related, and they both lived to old age.

Vision of LE. noticed to be defective six months ago. It could not be ascertained
with certainty whether this eye ever had good vision. About the same time he
experienced a difficulty in seeing in a dull light. V. RE. = f. LE. +2 D. = 9 Snellen
at 10 inches. Visual fields normal, both in a bright and in a dull light. The LE.
presented similar ophthalmoscopic appearances, but they were perhaps a little more
advanced.

Description. — The disc presents nothing abnormal. No diminution in the retinal
vessels. Choroidal vessels visible over whole fundus, but they are not nearly as
numerous as in Fig. 60. Many of them are pale, and some are white. This is especially
the case above the disc, and in several isolated round areas. A conspicuous round white
patch above the disc ; this appeared, on careful focussing, to consist of numerous white
vessels. There are several isolated superficial deposits of pigment, and in the upper part
a considerable speckling with fine pigment.

Sxcbseciuent History. — Seen in January 1892. No appreciable change.

Plate xxvii

PLATE XXVIII.

RETINAL ATROPHY WITH SECONDARY PIGMENTATION.

Fig. 62. — Atrophy of Retina with Secondary Pigment Changes.

Mary B., 77. LE. Drawing made in 1888. — Vision said to have been failing six months,
but no reliance could be placed on the history. The patient was of senile aspect, and weak
in intellect.

Description. — Fundus of the dull -red type. Disc dirty-looking colour. Arteries
reduced to threads and few in number. Veins also small. Choroidal vessels everywhere
visible as pale lines, except at the macula, which presents a normal appearance. Towards
the upper periphery dense masses of pigment, which seem to lie in the choroidal stroma.
There are also some superficial pigment deposits.

Plate xxviii

Fig. 62. LE

PLATE XXIX.

DIFFUSE CHOROIDITIS.

Fig. 63. — Diffuse Choroiditis. “Map-Like” Choroiditis.

Thomas S., 25. LE. Drawing made December 1889. — A tall delicate-looking man, but
without any history of bad health, or of definite illness. No history of syphilis.

First seen September 9th, V. = ^ He stated that LE. had been defective six weeks,
varying, but on the whole steadily getting worse.

The RE. appeared to be normal in all respects.

Ophthalmoscopic appearances in IjE. on September 9th. Fundus blurred, but no definite
opacities seen in the vitreous. Retinal veins much distended, but not tortuous. No swelling
of the disc. Above the disc a white, woolly area, with ill-defined margins, extending three disc
diameters from disc. In region of macula, indistinct white spots, and pigment disturbance.
In the lower and outward periphery, a large patch of choroiditis, which was thought to
be old. On December 6th (date of the drawing), Y. had improved to (4 letters). The
appearance of the fundus had greatly changed.

Description. — The disc margin is clear, the woolly patch above the disc and the changes
at the macula have disappeared.

Projecting inwards from the periphery on all sides towards the central area, but not
reaching it, are numerous pale areas, with a mottled surface. These are irregular in shape,
at the upper part they mostly form elongated islands in healthy fundus Below, the areas
are larger, and are separated, either by broad belts of normal fundus, or by narrow bands
which look like choroidal vessels. The latter are not visible anywhere in the healthy part
of the fundus.

Subsequent History. — On February 6th, 1890, Y. = f (2 letters), fundus unchanged.

Plate xxix

PLATE XXX.

RUPTURE OF CHOROID.

Fig. 64. — Rupture of Choroid.

Charles H., 15. RE. Drawing made January 1893. — Struck on the RE. with a stone on
December 31st. He was seen the same day. There was subconjunctival haemorrhage, the
pupil was dilated and inactive, Y. Ti% - 2 D = %. The ophthalmoscopic appearance was not
noted. On January 2nd the appearance depicted was discovered. V. was now £ without
glasses. On January 28th — Y. =£.

Description. — Midway between disc and macula an irregular white band, consisting of
two parts meeting each other at an angle. The upper has a few haemorrhages on its surface,
the lower is crossed by a band of pigment. The band measures at its widest part jV of
a disc diameter, and lies beneath the retinal vessels.

Above, and close to the disc, a few pale patches, mottled with pigment.

Subsequent History. — In June he found that V. was defective. When seen on July 2nd,
there was a small patch of dark colour at the macula. V. reduced to counting lingers,
and that only at the periphery of the field. More pigment on the edges and borders of the
pale band.

August 25 th. — Macula difficult to see, although no definite opacity was visible in the
media. The white band is now of steel-grey colour.

Fig. 65.— Rupture of Choroid.

Alfred E., 22. RE. Drawing made March 26 th, 1893, at which time V. was /£. Blow
on the eye on January 31st. When seen, three days later, pupil slightly dilated and
inactive. T~. Blood in vitreous. Fundus reflex, but no details, visible. V. = 24 Snellen
at 20 c.m. February lltli, a white band indistinctly seen on temporal side of disc. Y. = 12
Snellen at 20 c.m.

Description — To temporal side of the disc, a white band, broad below and narrow above,
roughly concentric with the disc margin ; further out, a shorter, nearly vertical band
connected with the first by a horizontal white line. Processes jut out from both vertical
bands, and between these are bays with sharply-cut concave borders. The bands are speckled
with fine lnemorrhages, and the lower part of the larger is crossed by choroidal vessels.
To the temporal side of both bands are three isolated white areas of long oval shape, which,
if joined, would form a line almost parallel to the long vertical band.

Plate xxx

Fig. 65. R E

PLATE XXXI.

PAPILLITIS.

Fig. 66. — Papillitis. Subsiding.

Annie T., 26 (married). RE. Drawing made July 24th, 1889. — First seen July 13tli,
stated that Y. of RE. had been noticed defective ten days, and was now improving.
V. RE. = jR2-, LE. = f. Two months ago she had a sore throat, followed by an eruption, which
has now disappeared. When first seen, the margin of the disc was more indistinct than
in the Figure, and the colour was nearly that of the fundus. There was also a small linear
luemorrhage downwards and inwards from the disc. She was treated with mercury, Y.
improved, and the disc became paler. On J uly 24th, the date of the drawing, V. of RE. = f .

Description. — The disc shades off gradually into the fundus without any distinct
boundary line. The retinal veins are somewhat tortuous. Some of the arteries are
accompanied by white lines.

Subsequent History. — August 20th — The disc presented a normal appearance.

Fig. 67. — Papillitis.

William R, 40. LE. Drawing made April
1889. — Vision of LE. failing six months.
No history or signs of syphilis. No cerebral
symptoms. Keflexes normal. Y. RE. = f ;
LE. — hand reflex. Visual field on April
13th as shown in the chart; on April 27th
it was normal. The drawing was made be-
tween these dates. RE. normal.

Description. — Disc swollen, of a greenish-
grey colour, margins blurred. The upper
veins are full, and make sinuous curves.
Near the superior nasal vein are two hemor-
rhages in the fibre layer. White lines accompany the lower vessels on the disc.

Stibsequent History. — January 1892 — Both discs were very white, there were white
lines accompanying the upper vessels in the left eye, Y. = T\ in each eye. Stated that six
months after the drawing was made he went to the Eoyal London Ophthalmic Hospital for
failure of the RE. The LE. at this time had, he believed, completely recovered. He
attended as an out-patient, but had lost his notes. The RE. recovered, and neither eye
has given him any trouble since.

PLATE XXXI .—Continued.

Fig. 68. — Papillitis. With Haemorrhages on Disc. Retention of Physiological Cup.

James G., 26. LE. Braiding made April 1892. — At Christmas he fell downstairs. He
was stunned for a few minutes. He did not vomit. The next morning he went to work as
usual, and had no symptoms for two or three weeks. He then complained of pain in the
head, for which he was blistered and treated in various ways without benefit for two weeks.
He then came under the care of Dr. Bell of Leystonstone, who has kindly furnished me
with particulars of the case. At this time he was suffering great pain, paroxysmal in
character, in forehead and occiput ; the severe pain would last for hours, and he succeeded
by slighter pain. There was insomnia, the bowels were constipated, and the tongue coated.
There was a foul-smelling muco-purulent discharge, mixed with blood, which appeared to
come from the naso-pharynx. Pupils equal, sluggish. Urine loaded with lithates ; patient
drowsy, and answering questions slowly. Treated with purgatives and bromide of
potassium. He improved, but the pain and discharge continued, and he was admitted into
St. George’s Hospital under Mr. Pick. The eyes were examined a few days after admission, and
papillitis with haemorrhages discovered in both eyes. Y. = £, in each eye. Visual fields normal.

Description. — Disc margin indistinguishable, except on the temporal side, where it is
quite distinct. Several striated haemorrhages. Veins dark and distended. No filling up
of the physiological cup.

Subsequent History. — The symptoms gradually subsided, and he was discharged. Seen
again December 1893. Has had no symptoms since his discharge. The optic discs appear
quite normal.

Fig. 69. — Papillitis. Disc much Swollen.

Silva T., 51. Drawing made June 1889. — No history of syphilis. V. of LE. failed
about three months ago, and that of the RE. soon afterwards.

For six months has suffered from vertigo, and constant pain in the left temporal and
occipital regions, with occasional vomiting. Has occasionally experienced numbness of left
side, and in left leg, and sometimes “ pins and needles ” in right arm.

When seen there was left facial paralysis, and the left ear was deaf. Knee-jerks normal.

V.<(To i11 each eye. The ophthalmoscopic appearances were similar in the two eyes.

Description. — Disc swollen, and “ woolly.” Paler than normal. Veins tortuous.
Arteries somewhat diminished in size. A small haemorrhage obliquely downwards from
the disc.

Subsequent History. — A month later — Giddiness, noises in the head, and pain, chiefly on
the right side of the head, have been nearly constant, but there have been no convulsions or
vomiting. Jour months later it was noted, “mental condition not very clear, talks
incoherently.” She was soon afterwards removed by her friends, and the result of the case
is unknown.

Plate XXXI

PLATE XXXII.

PAPILLITIS. POST-NEURITIC AND SIMPLE ATKOPHY.

Fig. 70. — Papillitis. With “ Ridging ” of the Retina.

Louisa H., 31. LE. Drawing made March 1890. — Admitted into St. George’s Hospital,
February 20th, for headache, from which she had suffered, off and on, for three years.
Said before admission to have had “ fits ” and twitching movements of the left hand.
While in the hospital there were occasional twitchings of the facial muscles ; it is not
stated on which side.

She was treated with mercury and iodide of potassium. During the two months she
was in the hospital the headaches improved, but the vision deteriorated.

The diagnosis of cerebral syphilis was made, but the notes do not give the evidence
on which it was based. Visual fields contracted. See charts.

LE. RE

V., March 8th. — EE. +3 I). = fq ; LE. +L75 D.= £. March 29th. — Each eye,

The ophthalmoscopic appearance of the disc was similar in the two eyes.

Description. — Disc swollen. Margin indistinguishable. Veins tortuous. Arteries
small. On the temporal side of the disc the fundus presents about eight parallel
horizontal light lines, giving an appearance as if the retina were thrown into folds.

Subsccpicnt History. — April 19th, both discs atrophic, the appearance resembling simple
atrophy, the margins being quite clear. Arteries diminished. Fields slightly smaller.
V., RE. = ; LE. — .

PLATE XXXII . — Continued.

Fig. 71. — Post-Neuritic Atrophy. Atrophy of Choroid near Disc.

Frances S., LE. 9. Drawing made October 1889. — An intelligent child. Y. failing
about a month. A specimen of her writing done a month ago was shown, and was
unusually good. Y. is now in each eye, and she is quite unable to read or write.
No general symptoms of any kind. No signs or history of inherited syphilis. RE.
disc atrophic.

Description. — Colour of disc greyish white. Outer margin sharply defined, the
remainder of the margin is indistinct. The choroid adjacent to the disc, except on the
temporal side, has undergone partial atrophy. The fundus generally has fine pigment dots
sprinkled over it. The retinal arteries are much diminished. The upper one is
accompanied on the disc by a white line.

Subsequent History. — The child was admitted into the Belgrave Hospital for Children
on account of fretfulness, believed to be due to some intracranial condition. No definite
symptoms, however, were observed while the patient was in the hospital. The further
history could not be traced.

Fig. 72. — Post-Neuritic Atrophy.

David C., 40. RE. Drawing made November 1889. — An agricultural labourer. Has
always lived in the country. Always had good health. Denies excesses of any kind.
No history of injury. About December 1887 vision gradually failed without pain,
headache, or other symptoms.

When seen V. RE. = and 6 Snellen ; LE. = -/-g- and P8 Snellen. Concentric contrac-
tion of both visual fields. Colour-vision very defective. Pupils act with convergence, but
not to light. No ataxic symptoms.

Description. — Nasal border of disc blurred ; temporal border clear. Whole disc
white, especially its outer half. The colour is a uniform dead white without stippling.
Veins distended, but not tortuous.

Fig. 73. — Simple Atrophy.

John B., 51. LE. Drawing made July 17th, 1889.

Gait ataxic. Knee-jerks absent. V. failing, gradually, six months; it is now

RE.- 19 Jaeger. LE. = hand reflex. Pupils noted as acting to light, but only feebly

with convergence.

Description. — Outline of disc hard and regular. Surface bluish-grey, slightly stippled.
No small vessels are visible. The large vessels are of normal size.

Plate xxxii

Fig 72. R E

Fig 73. L Z

PLATE XXXIII

LEUKiEMIC RETINITIS. PAPILLITIS.

Fig. 74. — Leukemic Retinitis.

Ada Smith, 26, single. RE. Drawing made December 6tli, 1892 — Always lived in
London. No history of syphilis or alcoholism. Influenza in June 1891 ; no other
definite illness. Father died of heart disease and phthisis. One brother died of

rheumatic fever and heart disease ; one brother, four sisters, and mother living, and
reported healthy.

Patient suffered for many months from shortness of breath, pain in chest, and
enlargement of abdomen.

Admitted to Westminster Hospital, December 8th, 1891, under Dr. Donkin. Rather
emaciated, slight dyspnoea. Temperature, 99 ; pulse, 96, soft. Spleen reaching from iliac
crest to cardiac dulness, ami beyond the middle line. Loud systolic bruit, loudest over
nipple. Urine 1025. No albumen or sugar. Catamenia scanty.

Blood corpuscles, 4,500,000 to sq. mm. Proportion of white to red, 1-4.

Improved and went out in a few weeks, but returned April 7th, 1892, having had
severe epistaxis. More emaciated. Spleen larger. Liver extending P5 ins. below costal
cartilages. In June diarrhoea several weeks. November 11th, 1892, further increase in size
of liver. November 24th, Y. RE. + 2'0 D=~w.

Description. — Disc margin indistinguishable, its centre indicated by an ill-defined
grey area, and by the converging of the vessels. General colour of fundus a trifle pale.
The veins distended to about four times the normal width ; the arteries, which resemble
them very closely in colour, are also somewhat dilated, being perhaps half as wide again
as in the normal condition. Both arteries and veins are extremely tortuous, and make
bold curves as they cross the position of the disc margin. At the summits of these
curves the light streak is unusually conspicuous. Some of the other curves also show a
brilliant light streak at their summit ; but in the upper temporal vein the light streak is
remarkably uniform and broad, but not brilliant. The whole fundus has a misty appear-
ance, and in places the vessels appear gradually to disappear into fog. Probably this
mistiness prevents any small vessels being visible

Subsequent History. — Became gradually worse, and died on January 29th.

Autopsy. — Veins generally full, the blood in them of a brownish colour, and most of it
clotted, the clot being granular, and partly of a yellowish colour. Numerous old pleuritic
adhesions. Greater part of lungs consolidated, of pi tiki sh -grey colour, friable. Mediastinal

PLATE XXXIII . — Continued.

glands very large. Liver, 162 oz., pale and soft. Spleen, 67 oz., fairly firm, “ beefy,” of
brick- red hue, on section shows a pyramidal yellow infarct. Except in size no material
difference from normal. The microscopical appearance of the fundi has been described in
the body of this work under the heading of “ leuksemic retinitis.”

Note. — This case, with a chromo-lithograph from the same stones as Fig. 74, has been published in Trans.

Ophth. Soc., U. Kingdom, London, xiii., p. 72.

Fig. 75. — Papillitis. Much Swelling. Vision Unaffected. Subsidence.

Kate H., 20, single. RE. Drawing made January 1893. — On December 7th, she fell and
struck the outer side of right orbit. Considerable ecchymosis followed. As soon as she
could open the eye, she noticed that all objects had appeared to have a trembling
movement. It was the annoyance caused by this that led her to seek advice on December
21st. V. was then f, and the visual field was normal. With the ophthalmoscope the
condition depicted was found. The LE. presented nothing abnormal.

The urine contained neither albumen nor sugar.

Description. — The disc is replaced by a grey, soft-looking area, shading off gradually
into the fundus, without any line of demarcation. This area is not less than three times
the normal disc diameter, and its surface has a distinctly striated appearance. With the
ophthalmoscope it could be seen to be considerably raised. Between the disc and the
macula are numerous hard, small, white dots, which near the macula appear to have
coalesced into four or five lines converging towards its centre. The veins are distended
and extremely tortuous. They make bold curves as they pass over the edge of the swollen
papilla. The convexities of their curves exhibit a strong light reflex ; the concavities are
often hidden from view in the retinal tissue, so that the continuity of the vessels appears
interrupted. The arteries show no change.

Subsequent History. — The patient was seen at frequent intervals for about four months.
During the first part of this time she was treated with mercury, and later with tonics. No
change took place either in the ophthalmoscopic appearances, or in the vision. She was
seen again in March 1894. All trace of swelling of the disc had disappeared ; its margin
was clear, except above and below, where it was a little fluffy. There were some fine bands
of grey tissue in front of the centre of the disc. The veins presented a normal appearance.
V. visual field normal.

Plate xxxiii

PLATE XXXIV

THROMBOSIS OF CENTRAL VEIN.

Fig. 76. — Thrombosis of Central Vein.

Mrs. Lyell, 35. LE. Drawing made March 2 Oth, 1894. — Seen February 13th, 1894
A year ago had erysipelas of left side of face, lasting a week. The LE. never as good as right ;
a week before visit it was noticed to be worse. It then remained stationary till two days
ago, since when it has been getting worse. RE. T*V + 1'0 D = £. LE. ^- + 2 D = -£x.

Urine acid — no albumen. Fundus of right eye normal ; LE. as depicted.

Description. — Disc margin indistinguishable. Veins distended and tortuous. Arteries
small, and few in number. Numerous htemorrhages in fibrous layer, becoming more
scattered towards the periphery. Downwards and outwards a white patch — -probably an
altered haemorrhage. Owing to rapid onset of vitreous opacity, a second sitting could not
be obtained, and the drawing is therefore somewhat incomplete.

Subsequent History. — The vitreous became too opaque for the fundus to be seen, and
remained so for many weeks. In September it had cleared. The vessels were as in the
drawing; there were fewer htemorrhages, but numerous white areas. December 4th — V. =
Veins still distended, but much less tortuous. Arteries small, and accompanied by white
lines. A few scattered haemorrhages having a granular appearance. A few fine vessels,
probably of new formation, on the disc.

Fig. 77. — Thrombosis of Central Vein.

Sarah S., 48. LE. Drav-ing made November 1892. — Vision of LE. said to have been
failing 18 months. V. LE. fingers; RE.

Has always had good health. Catamenia ceased two years ago. Urine showed a large
cloud of albumen.

Description. — Disc margin indistinguishable, no swelling of disc. The adjacent fundus
for a distance of about 3 del. covered with numerous striated haemorrhages. Beyond
this distance the haemorrhages become less abundant and are less distinctly striated,
many being quite irregular in shape. The extravasations are also irregular in the yellow-
spot region. The fundus between the haemorrhages has a yellowish tinge, and the disc
margin is occupied by an ill-defined broad band of lighter colour, which fades off gradually
into the fundus on the one side, and into the centre of the disc, which is abnormally red, on
the other.

The retinal veins are somewhat distended, and extremely tortuous. The convexity of
most of the curves shows the light streak very conspicuously, while most of the deeper
curves are hidden in the substance of the retina. The superior nasal vein, traced towards
the disc, appears to plunge almost vertically into the retina two disc diameters from the
disc, and to be invisible from this point. A much smaller vein joins the main upper vein
near the disc, but it is doubtful if this is the same vessel. There is a small arch formed by
a vein just below the centre of the disc. The perivascular sheath is seen along several of
the veins. Only a few arteries are visible. They show no alteration in size.

Subsequent History. — Could not be traced.

Plate xxxiv

FlO. 77. L.E

PLATE XXXV.

RETINITIS WITH HAEMORRHAGES.

Fig. 78. — Retinitis. Haemorrhages and White Dots. Recovery.

Jane R., 57. RE. Drawing made September 1889. — Y. RE.<-^. No reliable account
could be obtained as to the date of the failure ; LE. normal. No albumen in the urine.

Description. — No blurring of disc margin. Haemorrhages in the fibre layer near the
disc. Midway between disc and macula a white patch, surrounded by a granular-
looking haemorrhage. To the temporal side of macula another similar haemorrhage without
any white. A few isolated dark extravasations of blood. In the macular region numerous
small dots of chalky whiteness, which on the temporal side of the macula appear to have
coalesced into four or five lines, which converge towards its centre.

Subsequent History. — In March 1890 the haemorrhages had all disappeared, and left no
trace. In the region of the macula a few white dots only remained. Y. + 3 D = f.

Fig. 79. — RE. Retinal Hemorrhages. Thrombosis?

James T., 66. Drawing made March 1890. — Y. of LE. noticed defective in December.
The if A'.- failed soon afterwards. Early in January he was confined to bed with “ rheumatism
and cold,” and afterwards with influenza. V. RE. = ^. LE. = fingers.

Patient’s aspect very senile. Pulse hard. No albumen in urine.

LE. opacity of lens, which prevented a clear view of the fundus, but white patches
could be indistinctly seen.

Description. — Numerous haemorrhages scattered over the fundus, lying chiefly in the
fibre layer of the retina. The nasal border of the disc concealed by blood. No perceptible
swelling of disc. Several white patches, which are probably caused by changes in effused
blood. Both arteries and veins are small.

.Subsequent History. — Could not be traced.

Plate xxxv

PLATE XXXVI.

ALBUMINURIC RETINITIS AND NEURO-RETINITIS.

Fig. 80. — Retinitis at Macula. Hyaline Thickening of Artery.

Eliza R., 52. RE. Drawing made May 1892. — A stout woman. (Edema of feet only
after prolonged standing. Micturition rather frequent. Urine contains a distinct trace of
albumen.

Y. failing gradually two or three years, is now RE. = LE. =

In LE. a large haemorrhage on disc, extending about a disc diameter into the fibre layer
of retina, and a few small haemorrhages near macula.

Description. — Disc normal ; central light streak on arteries unusually well marked.
The inferior temporal vein, a disc-and-a-half or L5 dd. from the disc, is crossed by a small
branch of the corresponding artery. The artery has the appearance of passing through a
gap in the vein, which is larger than the visible diameter of the artery. On either side of
the gap the vein appears to terminate in a dark spot. The diameter of the vein is the same
on each side of the apparent gap. The lower half of the macula is embraced by a group of
chalky-white dots, arranged in lines converging towards the centre of the macula.

Subsequent History. — February 1893- — No haemorrhages. White dots fewer. Vessels
as before. V = |- each eye.

Fig. 8 1 . — N euro-Retinitis.

Samuel G., 17. LE. Drawing made September 1890. — Was admitted into St. George’s
Hospital from one of the Metropolitan Asylum Hospitals, where he had been a patient for
enteric fever. This was complicated with a mastoid abscess and facial paralysis, which had
recovered before admission. He complained of defective vision, and on ex. mination optic
neuritis in both eyes was discovered.

Perforation of membrani tympani of some years standing. No mastoid or temporal
tenderness. Adenoid tissue in naso-pharynx. The condition in the ear was thought to be
secondary to this.

On September 1st, V. RE. + 3 D = LE. + 2 Z> = T6T, hut on September 17th corrected
V. was £ in each eye. The visual fields were nearly normal.

The ophthalmoscopic appearances were similar in the two eyes.

Description. — Disc swollen and woolly-looking ; margin indistinguishable. Retinal
veins tortuous. Arteries small. Numerous soft-looking woolly patches. In the course of
the inferior temporal vessels, a large area of opaque retina. Chalky-white dots between
disc and macula, and around macula.

Plate xx xvi

PLATE XXXVII.

ALBUMINURIC RETINITIS.

Fig. 82.— Albuminuric Retinitis.

Samuel S., 33. LE. Drawing made January 1890. — He applied on account of failing
vision, which was RE. = LE. = Ti\. He had a typical renal aspect, and he was transferred
to the physician, who reported — “ Urine, sp. gr. 1010 acid, nearly solid from albumen. Heart
apex in 7th space in nipple line. Reduplication of first sound at apex, second sound
accentuated. Pulse hard. Much oedema of face and legs. Some fluid in abdominal cavity.”

The condition of the two eyes was similar.

Description. — Disc margin blurred, especially on temporal side. No swelling of disc,
white lines on the upper and lower veins on the disc. Between disc and macula a few
haemorrhages. Several white “ woolly ” patches. Small chalky dots near macula.

Subsequent History. — He was seen at intervals for a few months. His general condition
improved, but no appreciable change took place in the fundus. Early in 1891, on enquiries
being made, it was reported that he had died some months previously.

Fig. 83. — Retinitis. Without Implication of Disc.

Elizabeth S., 53. RE. Drawing made July 1889.

V. of RE. noticed defective a month. RE.<^~ and 16 J ; LE. = %.

Description. — Appearance of disc normal. Veins distended and very tortuous. This is
especially the case with the superior temporal, which in several places appears to dip into
the swollen retina and become hidden from view. The inferior temporal vein is also hidden
for a short distance a little way from the disc. The macula is normal. Above the space
between it and the disc numerous soft-looking, woolly white areas. Numerous luemorrhages,
of somewhat granular appearance.

Fig. 84. — Albuminuric Retinitis. “Star-Figure” at Macula.

George S., 58, a sexton. RE. Drawing made January 1889. — Dimness of V. noticed a
month. Now RE. = Tfi¥, LE. = Legs slightly oedematous. Pulse of high tension. First heart

sound reduplicated. Urine has been passed with undue frequency for some years. During
an attack of pleurisy some months ago it contained blood. Now sp. gr. 1012 albuminous.

Description. — No perceptible swelling of disc, but its margin quite indistinguishable.
A few flame-shaped htemorrhages near the disc. A few “ woolly ” patches on fundus.
Numerous small white dots round the macula. On the macula these appear to have
coalesced to form lines converging towards its centre.

The inferior temporal vein, where it is crossed by the artery, appears to present a gap
about twice as wide as is required for the passage of the artery, as in Fig. 80.

Subsequent History. — In February 1890 Mr. Fisher, of King’s Langley, under whose
care the patient was, wrote : — “ Six months ago he developed uraemia, and remained more or
less comatose for three weeks. He then gradually recovered but kept his bed, and his
eyesight remained very defective. Three weeks ago a second attack came on, and he died
in 48 hours.”

Plate xxxvii

Fig. 84. EE

Fig. 82. L.F

Fig, 83. E.E

PLATE XXXVIII.

STELLATE FIGURE AT MACULA AND POST-NEURITIC ATROPHY.

Fig. 85. — Stellate Figure at Macula of Unusual Character.

Lizzie B., 21. Drawing made July 21th, 1888. — First seen at St. George’s Hospital, on
July 11th. She stated that on July 6th she had experienced an uncomfortable sensation
in the left eye, as if from a foreign body, and that at the same time she noticed a fog
before the eye. Two days later the sight had improved, and it then remained the same
till her visit.

Patient somewhat anaemic. Has always been considered delicate, but does not
appear to have had any definite illness. She has suffered since childhood from severe
headaches, affecting the whole head, and usually accompanied by vomiting. These used
to come on every three weeks, and to last for two or three days. They have been less
frequent during the last two or three years, and during the past year she has had very
few attacks. Menstruation has always been regular. No constipation. Urine acid, no
albumen.

Y. HE. = f , LE. = JT. Visual field (roughly tested), normal.

The disc margin presented the striated appearance frequently seen in dark eyes,
but this was more marked than in the right eye. There was also some slight real
blurring. On the upper and outer quadrant of the disc a minute haemorrhage. The
retinal arteries were thought to be smaller than normal. As there was a suspicion of
embolism, the macular region would certainly have been carefully examined, but
nothing abnormal was noted at this visit.

At the next visit, on July 11th, Y. the same, and the appearance depicted was
discovered. The visual field was carefully tested and found to be normal for white.
There was a small scotoma for red (test object 3 mm.) below the fixation point.

Description. — Some retinal striation on upper 1 (order of disc, but elsewhere it was less
marked than before. The small heemorrhage on the disc still present. Retinal veins twice
the diameter of the arteries (in the other eye the proportion was 3 to 2).

The macula of dark colour, radiating from it in all directions an immense number of
fine hard lines. Each line was thicker at its centre than at either extremity, the
thickened portions corresponding in position with the oval reflex-ring often seen in this
region. The lines were appi’oximately a disc diameter in length. Beyond them, especially
above, numerous extremely minute white dots.

PLATE XXXVI 1 1. — Continued.

Fig. 86. — The Same Eye. Two Months Later.

The ophthalmoscopic appearances had much changed. V. still

Description.— The fine stride have disappeared, in their place a few short and thick
lines of chalky whiteness. The retinal dots are fewer and larger.

Subsequent History. — January 16th, 1889. Only a few dots round the macula, and a
few isolated dots between disc and macula. The disproportion between arteries and
veins no longer noticeable. V. = •§,

Fig. 87. — RE. Post-Neuritic Atrophy.

Edwin R, about 35. Drawing made May 1889. — The full notes of this case have
been lost. The patient, some months before, had been an in-patient at a general hos-
pital for symptoms believed to depend upon a cerebral gumma. He became blind while
under treatment there.

Description. — Veins tortuous, hidden in places on the disc. Arteries diminished.
Disc white, its margin indistinct, except on temporal side. A few chalky dots between
disc and macula. A haemorrhage downwards and inwards from disc.

Subsequent History. — It was ascertained that the patient was removed to a lunatic
asylum in 1892, and that he recovered sufficiently to be discharged in six months. In
April 1894 he was said to be suffering from frequent fits.

Plate xxxvni

Fig 85. L.E

Fig. 86 L.E

Fig 87 R E

PLATE XXXIX.

SUB-HYALOID HAEMORRHAGE.

Fig. 88. — Sub-hyaloid Hemorrhage at Macula.

Phoebe K., 63. RE. Drawing made April 12th, 1889. — On March 31st, whilst lifting a
patient, she noticed a sudden flash in the right eye. Since then vision has been dull, and
all objects have appeared red.

When seen, Y. = counting fingers. A central scotoma, having a radius of about 10°.
This corresponded with the changes in Fig. 89 rather than with those in this figure. LE.
normal.

Description. — Extending from a point half a disc diameter on the temporal side of the
disc to a-disc-and-a-half beyond the fovea D-shaped haemorrhage. The straight limb is
horizontal, and forms its upper boundary. The colour of the extravasation is deepest below ;
through the upper part the fovea centralis can be seen as a pale spot. Beyond the temporal
border of the extravasation a few haemorrhages.

Fig. 89. — The Same Eye. 14 Days Later.

IIE. Draiving made April 26th, 1889, but the appearances shown ivere discovered on
April Vltli. — Vision as before.

Description. — The shape of the extravasation is unaltered, the small haemorrhages
which lay beyond it have disappeared. Extending from the upper border of the haemor-
rhage to the superior temporal vessels is an area of grey colour, the surface of which shows
indications of striation. The surface of the grey patch as well as of the original extravasa-
tion sprinkled with very minute white dots, which had a highly refracting appearance.
Between the extravasation and the grey area are four large round white spots in contact
with each other.

Subsequent History. — On May 10th. V. +l-25 = f.

Not seen again till December 10th, 1892. Stated that V. had remained good till a few
days previously, when a sudden failure occurred. Ophthalmoscopic examination by the
direct method was difficult, as but little light was reflected from the fundus ; with the in-
direct method a large dark-grey area could be seen occupying approximately the site of the
extravasation in Fig. 88, but extending further to the nasal side, between this and the
inferior vein, a D-shaped haemorrhage, its straight boundary to the temporal side, and
inclined a little downwards and outwards from the vertical. Above the upper edge of this
a brilliant white crescent. This seemed to reflect the light very strongly, and had the
appearance of peeping out from behind the haemorrhage.

In January 1896. — Sudden failure of LE. to A nearly circular extravasation,
3 dd. above the macula, of uniform dark colour. In contact with its lower border a
dark grey cresentic area. Below this again — a strip of normal fundus intervening — a D-
shaped haemorrhage, with straight line nearly horizontal, and a very short vertical diameter.
In RE. pigment deposit and staining in macular regions. V. p.l. Still under treatment.

Plate xxxix

PLATE XL.

CHANGES IN VESSEL- WALLS. NEW VESSELS IN VITREOUS.

Fig. 90. — Degenerative Change in Arterial Walls.

Ann H., 43. RE. Drawing made July 1889.

Six months previously, in the eighth month of pregnancy, there was sudden loss of
vision in the LE., followed by gradual partial recovery. She has had three similar attacks ;
the last, which occurred a month ago, was not followed by any improvement. In the LE.
no definite opacity can be seen in the media, but there is only a faint fundus-reflex
obtainable. V. LE. no p.l, RE. = y-g.

Urine pale, acid. A well-marked cloud of albumen.

Description. — Inferior temporal artery in part of its course converted into a white band
of the width of the corresponding vein. In places, a thin blood stream is visible down
the centre. A small vessel passing upwards and outwards is entirely white, and the
inferior nasal artery is similarly affected on the disc. Two uniform-looking haemorrhages.
No changes at the macula.

Fig. 91. — New Vessels in the Vitreous.

Frances C., 54. RE. Drawing made November 1889. — First seen June 3rd for recent
failure of right eye, V. RE. = -/U LE. = jf. There was a haemorrhage in the macular region,
and a corresponding defect in the visual field, which was otherwise normal. Urine pale,
cloudy, sp. gr. 1022. Faint trace of albumen. Patient suffers from headache, giddiness, and
oedema of feet.

On November 12th, V. RE. Tc-g. The ophthalmoscopic appearances depicted were
discovered.

Description. — Several of the retinal vessels have white lines accompanying them on
either side, and some of the smaller ones appear as white bands. There are several small
luemorrhages, one below, of a peculiar feather-like shape. A few soft white patches on the
retina. Springing from the disc are numerous fine vessels. The majority of these lay in
a plane anterior to the disc (2‘0 D). Some appear to have at their distal extremities
swellings of the same colour. Most of these latter were ill-defined, and had the appearance
of haemorrhages, but the shape of others suggested that they were composed of the closely
packed convolutions of a fine vessel.

Subsequent History. — In January 1890 the vessels were accompanied by a thin gauze-
like membrane which was sharply limited below, but shaded off gradually above. There
was a smaller bundle of new vessels on the inner side of the disc.

The vitreous soon afterwards became opaque. But in May 1892 it had partially
cleared, and the fundus could be seen indistinctly. Upwards and inwards from the disc a
brilliant white membrane could be seen with some vessels on it. It appeared to be too
smooth for a detachment of the retina.

Plate XL.

Fig. 91 EE

Fig. 90. R E

PLATE XLI.

EMBOLISM OF CENTRAL ARTERY.

Fig. 92. — Embolism of Central Artery.

Emma T., 50. RE. Drawing made November 13th, 1888. — Three weeks after discovery
by the patient of the loss of vision.1

First seen on October 26th. Stated that on October 21st she had had a slight fall,
to which, at the time, she attached no importance. On waking on the morning of the 23rd,

she discovered that she could only with the
RE. distinguish light from darkness, and she
experienced a sensation of fulness over the
right brow.

At the age of nine she had rheumatic
fever ; this was followed by chronic pains in
the limbs for three or four years. From eleven
till fifteen she lived at Charlton, near Wool-
wich, and had several attacks of ague, followed
by chorea, affecting the right arm and leg, and
the speech a little. At twenty-eight, she had
rheumatic fever again, and diphtheria, and was
confined to bed five weeks. At forty-two she
had another attack lasting two weeks, and
another lasting five weeks a year ago. She
has since had chronic pains in legs. Two months before her visit, she found one morning
on waking that she had a difficulty in speaking — this lasted a month.

For a long time she has suffered from palpitation and shortness of breath on exertion.

A loud mitral systolic murmur, slight oedema of feet and ankles. V., hand movement
only, and this over a very limited area ( see Chart).

Description. — Disc of normal colour ; retinal veins unusually dark, their size is
approximately normal, but they become smaller on the disc. No venous pulse could be
produced by pressure.

1 The patient was under the care of Mr. Hartridge, to whom I am indebted for the notes of the case, and for
the loan of the original drawing.

PLATE XLI . — Continued.

The width of the blood stream in the arteries is much diminished ; in several the
artery is replaced by a white band, with a narrow thread of blood visible down its centre.
In the macular region a whitish area, in which the macula is seen of its normal colour,
with a minute fovea centralis. There are haemorrhages on and near the disc.

Subsequent History. — In July 1890 the macular region appeared normal. The disc was
atrophic. V. = no p.l.

Fig. 93. — Embolism of the Central Artery. Modified by the Presence

of a Cilio-Retinal Vessel.

Henry T., 40. LE. Drawing commenced July 18 th, 1893, 44 hours after the loss of V. ;
and completed the following day.

First seen July 17th; stated that twenty-four hours previously he had suddenly lost
the sight completely (no pi.) in both eyes. In a few minutes the sight returned to the

RE., but the LE. remained blind. The attack
was accompanied by a feeling of faintness.

A rather anaemic, nervous man. He had
rheumatic fever twenty years ago; does not
know that his heart was affected. Heart
sounds normal. V. RE. — 2 I? = - 1 ; visual field
normal. LE., can just see hand movements
over a small area of the field, extending from
the fixation-point to the blind-spot. See chart.

Description. — The whole fundus, except an
area on the temporal side of the disc, of a
whitish colour, only faintly tinged with red.
The disc margin, except on the temporal side,
is indistinguishable. The size of the retinal
vessels is normal, the light-reflex is absent from
some of them. In the centre of the macular
region is a brilliant red spot, looking like a luemorrhage, round this a light band, and round
this latter again a broader dark band. Between the disc and macula an irregular area of
normal coloured fundus, rather abruptly limited above, but shading off gradually below.
This is crossed about its centre by a small (cilio-retinal) vessel, which emerges from the
temporal border of the disc. Near the macula are several pale bands on this normal
area, which converge towards the macula.

Subsequent History. — Some months later the disc had undergone white atrophy, and
there was no p.l. The upper arteries were small, especially near the disc.

E XLI

PLATE XLI I.

RETINITIS PIGMENTOSA. PIGMENTATION FROM CHOROIDO-RETINITIS.

Fig. 94. — Retinitis Pigmentosa.

Alice M., 23. LE. Drawing made August 1888. — Patient is the third of five children.
Both parents living and reported healthy ; they are not blood relations. None of the other
children are known to have defective sight. The eyes of one brother and one sister were
examined and found normal.

Patient presents no sign of inherited syphilis. There is no history or probability of
the disease having been acquired. She has little colour, but is not markedly amende. She

is not considered strong, but has had no definite
illness.

The defect in the vision of the LE. was
first noticed in January 1887, after an inflam-
matory attack (conjunctivitis ?). Since then
it has altered a little, if at all. She was not
conscious of any defect in the RE.

First seen March 1888. V. =-§- in each
eye. The visual field of the RE. normal, that
of LE. as shown in the chart. In answer to
questions, patient said that she saw worse at
night, hut the difference does not seem to have
been very marked, and the visual acuity
was not lowered disproportionately on dimin-
ishing the light. With Forster’s photometer,
however, there was marked diminution of
the light-sense in both eyes, but especially in the left.

In the RE. were some isolated pigment streaks in the periphery of the retina, some of
them accompanying the vessels. The disc of normal colour, surrounded by a pale band.
The vessels of normal calibre.

Description. — Disc has a dirty-looking colour. Retinal vessels rather small. Towards
the periphery the characteristic network of pigment. Beneath the pigment network the
choroidal vessels are visible to an abnormal extent. At the extreme periphery the fundus
seemed rather less pigmented, but the choroidal vessels were more visible. Below the
macula is an area of partial choroidal atrophy, with a rather dense pigment deposit.

S ubsequenl History. — Patient seen at intervals till November 1894. There were fluc-
tuations in the vision (at one time it went down to -£$), but no permanent alteration. No
appreciable change occurred in the ophthalmoscopic appearances in either eye.

PLATE XLI I • — Continued

Fig. 95. — Choroido-Petinitis. With unusual Pigmentation.

Charles W., 37. RE. Drawing made May 1889. — Patient is a Eurasian, employed in
Government service in India. Seven years ago he had a chancre. He was treated with
mercury. No secondary symptoms followed. He married shortly afterwards, and has had
three children, which are said to be healthy.

Four years ago he had an inflammatory attack in the RE., which he believes did not
permanently affect the sight. Three years ago, on returning to India after a year’s furlough,
the sight of the right eye failed rapidly, falling to perception of light only in two weeks.
It has remained in the same condition since. The left eye began to fail about the same
time, but more gradually, and with fluctuations. At the date of the drawing Y. RE. pi.
slight concentric contraction of the visual field. LE. TeT. The condition of the fundus was
similar in the two eyes. In the LE. there were fine dust-like opacities, and a few films, in
the anterior part of the vitreous.

Description. — Fundus of the dark sombre type. Disc normal. Choroidal vessels
visible as pale streaks. Numerous irregular spots of pigment, showing no tendency to form
a network.

Subsequent History. — Treated with mercurial inunction, and iodide of potassium
internally, with intervals, for six months. V. of RE. was then unaltered, that of LE. = ~.
The visual field of LE. was normal. No change in the appearance of the fundi. He
returned to India shortly afterwards.

Flate xlii

PLATE XLIII.

RETINITIS PIGMENTOSA.

Fig. 96. — Retinitis Pigmentosa.

James D., 35. LE. Drawing made 1889. — First seen, August 1885. Patient has black
hair, and moderately dark complexion. Is rather anaemic. Parents not blood relations.
He stated that his sight had been failing gradually for ten years. At first the defect was
only noticed at night, and it has always been worse then.

In 1879 he attended Moorfields for iritis. From his notes it does not appear that the
ophthalmoscope was used, and his Y. was noted as c. - 2'0 D = ~.

When seen in 1885, Y. c. - 2'0 D = On the capsule of each lens a thin layer of
buff-coloured opacity of irregular shape, and presenting numerous gaps. Visual field
contracted. Marked night-blindness.

At the date of the drawing Y. - 2-0 D = T6g-.

The fundus was similar in the two eyes.

Description. — Disc somewhat pale, having an opaque appearance, difficult to describe
or to depict, the margin softer than normal. Over the whole fundus the choroidal vessels
are visible, the spaces between them are dark and mottled. Towards Hie periphery nume-
rous branching lines of pigment forming an irregular network. The inferior nasal vein
has a pigment streak in contact with it for some distance.

The retinal vessels, both arteries and veins, are reduced in size.

Subsequent History. — Was seen at intervals till October 1895. No appreciable altera-
tion took place.

PLATE XLI V.

RETINITIS PIGMENTOSA.

Eig. 97. — Retinitis Pigmentosa. With little Pigment Deposit.

James C., 35. BE. Drawing made February 1889. — Stated that he had always been
slightly short-sighted. For the last two or three years he had noticed much difficulty in
seeing at night.

Y. BE. — 2'25 D = ^q) LE. — 3‘0 D = ^T. Visual fields contracted.

LE. RE.

Patient’s parents were not blood relations. He has two brothers, who are stated
to have no affection of the sight.

Description — Disc dull and waxy-looking, like dirty parchment. The superior and
inferior nasal arteries are only slightly diminished in size. Of the superior vessels only
the nasal branch is visible, and the diameter of this is about half the normal. Over the
whole fundus the choroidal vessels are visible, separated by grey mottled spaces as in
Fig. 96. In the lower and outer quadrant are several irregular pale areas speckled
with pigment dots.

Towards the periphery are branching lines of pigment; the shape and disposition
of these suggests that they follow the bifurcations of blood vessels. A vein on the
temporal side is covered with pigment for a considerable distance.

■

Plate xliv.

Fig. 97 E E

PLATE XLV.

CICATRICIAL BANDS ON FUNDUS.

Fig. 98. — Choroiditis. Secondary Pigmentation of Retina.

Formation of Cicatricial Bands.

Harriet D., 41. RE. Drawing made September 1888. — LE. opacities in lens, fundus not
seen. Sight of RE. said to have failed suddenly nine years ago ; to have improved, and then
to have slowly deteriorated. The history, however, was variously given on different
occasions, and is probably unreliable. No history of syphilis. Has had ten children, said
to be all healthy. V. = -£%. Visual field contracted chiefly above.

Description. — Disc waxy-looking as in Figs. 96 and 97, and encircled by a wide pale
band.

Choroidal vessels visible over lower part of fundus. In the lower and outer
quadrant a large deeply pigmented area. The pigment appears thickly massed without any
definite arrangement. Near the disc is a sharply defined area entirely free from pigment.
Passing horizontally inwards from the disc, a white band with almost parallel sides. Above
this, a similar band, partly covered by pigment. On the temporal side of the disc beyond
the unpigmented area, a similar band which has a choroidal vessel lying on it. A fourth
hand passes upwards and outwards from the disc, starting by the union of two processes,
and terminating peripherally in a small circular spot.

Subsequent History. — Seen again January 1896. LE. lens opaque, pigmented lymph
on capsule. V. p.l. The conditions in RE. seem unchanged, except that there was perhaps
more pigment on the white bands. V. = Ay.

Fig. 99. — Cicatricial Bands on the Fundus.

Annie Gr., 19. LE. Drawing made February 1889. — First seen December 1888. Applied
on account of recent failure of vision. The LE. had always been defective and diverged.
V. fingers. Ptosis of this eye only.

The failure of the RE. seem to be due partly to paralysis of accommodation.
V. 36e +2R Z> = xV + 5 D = 0-3 Snellen.

Description. — Disc normal. A pigment ring on lower and outer margin. Three white
lines diverging from the disc, that on the nasal side spreads out fan-wise towards the
periphery. Downwards and inwards, two smaller bands not reaching to the disc. One
ends in round white area, exactly like the upper band in Fig. 98. They all lie beneath the
retinal vessels.

Subsequent History. — Under antisyphilitic treatment the accommodation recovered,
and on March 3rd, V. without glasses was and 03 Snellen.

On April 3rd, she returned, accommodation having again become paralysed three days
previously. By June 5th it had again recovered. There was no reason to suspect the use
of a mydriatic.

Two weeks later, she was admitted into the medical wards for loss of power in right arm
and leg, and right facial paralysis. She left the hospital much improved, and has not been

seen since.

Plate xlv

Fig- 99 L.E.

PLATE XLVI.

DETACHMENT OE THE RETINA.

Fig. 100. — Detachment of the Retina.

Helena A., 20. LE. Drawing made November 1888. — In January 1887 she was struck
violently in the LE. by a cork from a soda-water bottle. As soon as she could open the eye,
all objects appeared red. A few weeks later she noticed that the lower part of the field was
defective.

When seen two months later V. BE. = 4 ; LE. = ~. Lower part of visual field deficient.
See chart.

A fine network of opacities in the anterior part of the vitreous. Upper part of retina

detached. The summits of the folds visible
with -f-4 D.

At the time the drawing was made the
conditions had not appreciably altered.

Description. — Only the upper part of the
fundus is shown. The disc would be situated
about a-disc-and-a-half below the margin of
the drawing. The upper two-thirds of the
drawing show the retina floated forwards. It
has a greyish colour, some red being faintly
seen through it. The white lines are due to
the light being reflected from the summits of
the folds into which the retina is thrown.

Subsequent History. • — The condition re-
mained without appreciable change till February
1888, when the vitreous became more opaque.
In July 1893 the lens was opaque, and no fundus reflex could be obtained. Punctate
opacities on the lower part of cornea. V p.l.

Fig. 101. — Detachment of the Retina.

Andrew H., 38. LE. Drawing made November 1889. — First seen September 1888.
LE. thought to have always been inferior to RE. Three days ago a “ dark cloud ” came
over the LE., which cleared off after four or five hours, but left the vision more defective
than before. In the upper part of the fundus there was a large white area, of triangular
shape, with its apex towards the disc. It was doubtful whether this was due to oedema

PLATE XLVI. — Continued.

or to detachment. Y. BE. = £ , LE. = Refraction not myopic. The condition remained
unchanged for several months, except that a few opacities appeared in the anterior part of
the vitreous. The patient was then lost sight of till November 1889, when Y. was only p.l.
and the fundus presented the condition depicted.

Description. — At the lower part are two dome-like detachments of the retina. The
detached retina looks thin and gauze-like, allowing a considerable amount of red reflex to
be seen through it. It is thrown into parallel folds, the summits of which, catching the
light, appear like opaque white bands. At the upper part of the picture an old opaque
detachment is sketched in, the bagging downwards of this is seen where the vessels curve
round its lower border.

Subsequent History. — In 1895 the media were too opaque for any view of the fundus to
be obtained. The other eye was still normal.

Fig. 102. — Detachment of the Retina.

Charles W., 16. Drawing made November 1889. — Good vision in both eyes till he
received a blow on one eye a few months before he was seen. Some days elapsed before
he could open the eye, and he then found that its vision was defective, and it subsequently
became gradually worse.

Description. — A very extensive detachment at the lower part of the fundus. The
detached portions are more opaque than in Figs. 100 and 101, but a faint fundus reflex is
visible through the more peripheral part. The gap between the two detached portions
became narrower towards the periphery.

Fig. 103. — Detachment of the Retina.

Ann C., 56. LE. Drawing made March 1889. — Stated that she had always been
short-sighted. Five or six months ago she noticed a dimness in LE., which gradually
increased. V. RE. - 8 0 D. = ; LE. p.l. Refraction, high myopia.

Description. — A very extensive dome-like detachment of the retina at the lower part
of the fundus. A faint fundus reflex visible through it.

Plate xlvi

Fig 102

Fig 103. L.E

PLATE XLVII.

COLOBOMA OF DISC. GLAUCOMA SIMPLEX.

Fig. 104. — Partial Coloboma of Disc.

Mary S., 15. LE. Drawing made August 1889. — A healthy looking girl. No signs of
inherited syphilis, and no likelihood of the disease having been acquired.

The BE. had been defective as long as the patient can remember. There were large
areas of choroidal atrophy. The physiological cup on the disc appeared to be filled up with
a material which could not be well defined with the ophthalmoscope.

The LE. (that depicted) V. = £. Visual field normal.

Description. — The disc is of unusually large size. The greater part of it is deeply cupped.
The uncupped portion forms a crescent widest above ; its limbs pass round the disc
forming a ring which becomes very narrow on the lower and outer border. The vessels
curve abruptly over the well defined edge of the cup. The floor of the cup presents on
its temporal side a white crescent. On the upper and inner side of, and in contact with,
the disc, is a patch of partial atrophy of the choroid.

Fig. 105. — Glaucomatous Cui>.

Alfred H., 41. LE. Drawing made 1888. — In the winter of 1879-80, after exposure to
bad weather, he became suddenly blind whilst driving. There was no pain, and the
sight returned in about three hours. In the spring of 1882, after much anxiety, the
sight of the left eye gradually failed, the failure being accompanied by halos round a
light. In the winter of 1883-4 there was gradual failure in both eyes with pain in
the eyes and head. Mr. Streatfeild performed iridectomy on the LE., and a few months later
on the BE. The operations were followed by considerable improvement, so that he
could read and write. Vision has, however, gradually failed since.

Description.— Disc oval, surrounded by a halo of choroidal atrophy. The whole disc is
cupped, the larger vessels bending abruptly over its edge. The floor of the cup has a some-
what greenish tint, and is stippled.

Fig. 106. — Glaucomatous Cup.

Thomas S., 46. BE. Drawing made October 1888. — First seen December 1887. Vision
failing gradually two or three years, more rapidly the last year. No pain in the eyes, but
occasional frontal pain. Both sclerotics were of a bluish grey colour. Although the
patient did not look older than his years, there was a complete arcus senilis in both eyes.
This formed a sharply defined ring, about a millimetre wide, and extending right up to the
sclero-corneal junction. BE. = ~T ; T + 2. Inner half of visual field lost ( see Chart).
IjE. + 2'25 D = L'-j ; T.n. Visual field normal. The ophthalmoscopic appearance in BE. did

PLATE XLVII. — Continued.

not differ appreciably from that which it presented at the date of the drawing.
LE. normal. Treated with eserine.

At the date of the drawing V. of RE. had
fallen to hand reflex.

Description. — Whole disc deeply cupped,
the veins curving abruptly over its sharp edge.

It is surrounded by a narrow zone of
choroidal atrophy; through this, below, there
emerges a small vessel. The arteries do not
dip into the cup.

Subsequent History. — Shortly after the
drawing was made iridectomy was performed
in both eyes. In March 1894, field of RE.
was worse ( see Chart), LE. still normal. In
December 1894 the lens was
turbid.

Fundus of

becoming

Fig. 107. — Glaucomatous Cup.

James B., 57. Draining made 1888. — Vision of RE. began to fail very gradually six
years ago. At first there was slight aching pain. He used some “ eye- water ” (atropine ?)

Description. — Disc deeply cupped in i
its sharp edge. Surrounding the disc a ba

after which he had rapid failure of vision, with
severe pain. Mr. Little of Manchester per-
formed a large iridectomy which completely
relieved the pain, but was not followed by any
improvement in the sight.

Three years ago the LE. began to fail, Mr.
Little performed iridectomy on this eye and
there was some improvement in the sight.

When seen Y. RE. was only hand reflex,
and the field could not be taken. With LE.
he could read 16 J. The field in this eye was
deficient above, the defect reaching nearly to
the horizontal ; the retained portion of the field
showed no contraction {see Chart).

The drawing is believed to represent the
right disc.

whole extent, the vessels curve abruptly over
i of choroidal atrophy.

Plate xlvii

Fig 10 4. LE

Fig. 105 L.E

Fig. 106.E.E

Fig. 107.

• ■

INDEX.

Abadie, recurrent intraocular h£emorrhage,
Abscess, cerebral,

„ of orbit,

Acromegaly causing optic atrophy,

Acute retro-bulbar neuritis,

Adams, J. E., late changes at macula
embolism, ....
Albinism, appearance of fundus in,
Albuminuria, retinal vessels in, .
Albuminuric retinitis (see Ketinitis),
Amyloid bodies on optic disc,

Anaemia causing optic neuritis, .

„ „ retinal haemorrhage,

Aneurism in cavernous sinus,

„ of retinal arteries,

Angelucci, thrombosis of vena centralis,
Angioid streaks on fundus,

Anophthalmos,

Apoplectic retinitis, .

Areolar choroiditis,

Arterial circle of Haller,

„ pulsation,

„ sclerosis,

Arteries (see also Blood Vessels).

„ choroidal,

„ ciliary,

„ „ rupture of,

sclerosis of, 106 ; xxvi.

retinal,

172
124
124

151

127

177

138, 160
137
203
124

167
124
162
187
210

168

102

30
60

161 ; xl.90

60 ’

15
15

. 113

xxvii. 61
48

aneurism of, . .162

„ „ “copper wire, ’’appearance of, 139

,, „ distribution of, . . 48

„ „ embolism (which see), . 174

,, „ hyaline thickening of,

139, 160 ; xxxvi. 80 ; xxxvii. 84
,, „ in albuminuria, . 139, 160

„ „ in glaucoma, ... 60

„ ,, in leuksemic retinitis, 195; xxxiii. 74

„ „ in optic atrophy, . 148, 155

„ „ in retinitis pigmentosa, . 207

„ „ light-streak in, . . 47

„ „ thrombosis of, . . 174, 179

,, „ tortuosity of, . . 51

Astigmatism, appearance of disc in, . . 45

i /yvj ru

Atrophic stage of choroiditis, 90, 96 ; xvi. 4„ ; xvii. 43

Atrophy of disc (see Optic Atrophy), . . 147

Bacillary layer of retina, .... 20

Barlow, tubercle of choroid, . . . 104

Barrett and Lang, cilio-retinal vessels, . 53

Becker, coloboma, . . . . . 71

Benson, coloboma of choroid, with entire iris, 71
„ „ of disc, .... 80

„ embolism modified by cilio-retinal

vessel, . . 53, 186

„ „ recovery, . . . 179

„ rupture of choroid, . . . 112

,, tortuosity of retinal vessels, . . 56

„ and Story, aneurisms on retinal arteries, 162
Berlin, commotio retinae, . . . . 218

Bird and Schafer, anatomy of macula, . . 64

Birnbacher, embolism modified by cilio-retinal

vessel, 35, 186

Blood in leukaemia, . . . . .195

„ in retinitis proliferans, . . .183

Blood vessels (see also Arteries and Veins).

„ choroidal, in albinism, . . 17

,, „ in dark cundi, 18; iii. s

„ „ in light fundi, 17 ; iii. y

„ ,, sclerosis of,

cilio-retinal,

106 ; xxvi. so ; xxvii.
50 ; vi. 15 ; xix. ,

,, frequency of, . . 53

„ in embolism, 53, 186; xli. 93
ciliary (see Arteries), . . 15

of optic nerve, . . . 31

in the vitreous, . . 163 ; xl. 91

retinal distribution of, . 36, 48, 49

„ „ in albuminuria, 138, 160

„ „ in leukaemia, . 195

„ ,, in optic neuritis, . 119

„ „ inretinitis pigmentosa, 207

,, „ in syphilis, . . 162

„ „ light-streak on, . 47

„ „ pulsation in, . 60

„ ,, sclerosis of, 161; xl. 90, 91

„ „ size of, . . 47

„ „ thrombosis of, 178

224

INDEX.

PAGE

Blood vessels, retinal distribution of, . . 48

„ tortuosity of, 51, 55 ; vii. 18, 19 ; xxi. 4g
Bock, coloboma, . . . . . 69

Borysiekiewicz, anatomy of retina, . .21,23

Brailey and Edmunds, blood vessels in

albuminuria, ..... 138, 160

Bristowe, hypermetropic disc, ... 42

„ retinal reflexes, . . . . 26, 65

Bull, Stedman, prognosis in albuminuric

retinitis, .....

139

Campbell, Kenneth, equatorial rupture

choroid, .....

113

Capillaries of choroid,

Carmalt, new vessels in vitreous,

165

Carpenter, tubercle of choroid,

104

Cataract, posterior polar,

101,

207

„ secondary to choroiditis,

101

,, „ detachment,

217

„ ,, retinitis pigmentosa,

207

Cavernous sinus, aneurism in,

,, ,, thrombosis of, .

124

187

Cellulitis of orbit causing papillitis,

124

Central choroiditis ( see Macula), .

64,

102

Cerebral affections causing papillitis, .

127

Chiasma optica, ....

29,

114

„ „ pressure on,

150

Choked disc, .....

121

Cliorio-capillaris, ....

Choroidal halo in glaucoma, 157 ; xlvii. 105, T06, 107

,, „ in retinitis pigmentosa, . 207

„ ,, in secondary optic atrophy, 155; xlv. P8

„ „ in old people,

. 98 ; xxiv. 56

Choroid, anatomy of, .

,, hypersemia of,

„ rupture of, .

. Ill ; xxx.64,65

„ vessels of,

“ Choroide Tigree,”

18; iii. 8

Choroiditis,

89 ; xv. 40, &c.

,, atrophic, .

90, 96 ; xxiii. 53, 54, 55

„ causes of,

109

„ central,

102 ; xxii. 49, 50, 51, 52

„ circumscribed, .

91, 103

„ classification of,

,, complications of,

„ course of,

„ diffuse,

106 ; xxix. 63

„ disseminated, .

,, exudative,

. 90 ; xx. 4fi

„ following concussion of eye, . 113

„ papillitis, 98; xxiv. 57; xxxii. 71
irregular pigmentation in, 95 ; xlii. 95
retinal affections in, 98, 99 ; xxv. 58, 59
senile, . . . 102; xxiv. 56

serous, ..... 89

suppurative, . . . . 90

syphilitic, . . . . 109

PAGE

Choroiditis, tubercular, . . . . 109

Choroido-retinal sclerosis, 106 ; xxvi. 60 ; xxvii. 61
Cicatricial changes in retina, . . 143 ; xlv. 99

,, ,, „ following cho-

roiditis, 112,

144; xxv,

,, ,, „ following neuro-

retinitis, 135 ; xxiv. 57
,, ,, in myopia, . . 143

Ciliary arteries, . . . . . 15

,, „ rupture of, . . . . 113

59 ’ Xlv-9S

Cilio-retinal vessels,

sclerosis of,. 107 ; xxvi. 60 ; xxvii.

50 ; vi.

15 ’

■ 45

,, ,, frequency of,

,, „ in embolism, 53, 186 ; xli. 93

Clarke, E., new vessels in vitreous, . . 165

Cloquet, canal of, ... 59, 75

Coccius, new vessels in vitreous, . . 164

Collins, Treacher, symmetrical changes at

macula,

Colloid degeneration of pigment layer,
„ „ at macula,

Coloboma of choroid, .

„ „ iris,

,, in unusual positions,

,, of disc, . . 79

,, „ macula, .

Commotio retinae,

Congenital crescent, 75 ; iv. 9, 10

„ „ above disc,

„ abnormalities,

Connective tissue after papillitis,

,, „ in retina,

,, „ ,, vitreous,

„ ,, on disc, .

„ „ ring, . . 43 ; i.

IX.

192
202
202
26’ 27

; viii. 25 ; xlvii. 104
. 103

. 218

vl- 15’ 16’ 17 ’ v^; 18’
19’ 20’ 21 ’ vm- 22

• 79; viii. 23

. 148

99, 143 ; xxv. 59
. 145

/ 5 ; xii. 32, 33

connection with con-
genital crescent,

2 ’

» » „ exaggerated, 43,84; v.14; viii. 24

„ ,, round central vessels, . 33, 38

Contusion as a cause of choroiditis, . 105, 113

Crescent, congenital, . . .75; vi., vii., viii.

„ myopic, . . . 97 ; xxiii. 53, 54, 55

“ Crick” dots (see Gunn’s Dots), . . 199

Crystalline bodies in retina, . . .135

Cupping, atrophic, . . . . .154

„ glaucomatous, . 156 ; xlvii. 105, 106, 107

physiological,

34 i 1> 2’ 3 ’ X^- 30’ <^C-

Dahrenstadt, stellate figure at macula, . 136

Dark fundi, 16, 17, 25 ; iii. 8 ; vi. 16, l7 ; x. 29 ; xlii. 95
Descending atrophy, . . . . .149

„ neuritis, . . . . .121

Detachment of retina (see Retina), . . 213

Deutschmann, choked disc, . . .122

Developmental Irregularities, . . . 68

INDEX.

225

Development of eye, .

Diabetes, new vessels in,

Diabetic retinitis,

Diffuse choroiditis,

Dimmer, light-streak on vessels,

,, macula,

„ retinal reflexes,

Disc ( see Optic Disc),

Disseminated sclerosis,

Dodd, pigmented moles on retina,
Dolganoff, coloboma on disc,
Doyne, pigment streaks on fundus,
Drusenbildungen on disc, .

PAGE

163

141

106; xxix. 63
48
63
26
28
151
19
84
211
. 203

Eales, embolism, recovery during examina-
tion, . . . . . .181

„ recurrent haemorrhage in young men, 172
Edmunds, blood vessels in albuminuria, 138, 160
,, ,, in leukaemia, . . 198

Elschnig, embolism, pathological examination, 180
Embolism, . . . . .174; xli. 92

,, causes, . . . . .178

,, late changes in, . . . . 177

,, modified by cilio-retinal vessels,

53, 186 ; xli.

,, recovery after, ....

,, symptoms, ....

Enlargement of ophthalmoscopic image,
Entoptic appearance of vessels at macula,

„ „ ,, retina (Purkinje’s

figures),

Erysipelas, causing retinal thrombosis,
Exophthalmic goitre, .....
Exudative choroiditis, ....

Facial vein, anastomosis with orbital veins, .
Forster, areolar choroiditis,

Fovea centralis (see also Macula),

,, „ anatomy, ....

,, „ ophthalmoscopic appearance,

65 ; ii. 4, 5, 6 ; iv.
Friedenwald, interrupted blood column in
retina, ......

Fuchs, congenital crescent,

,, retinitis circinata, ....

Fundus, gauge for, .....

„ normal appearance of, .

183

174

188

187

102

173

142

Glaucoma, . . . 155 ; xlvii. 79g,

Gould, hereditary optic atrophy, . . 153

Gowers, albuminuric retinitis, . . .137

,, embolism, pathological examination, 180

„ sheaths of optic nerve, ... 30

„ “ waxy ” atrophy of disc, . . 155

Graefe, embolism, pathological examination, 180
Granular layers of retina, . . . . 20

Griffith, leukaemic retinitis, pathological ex-
amination, . . . . . .197

PAGE

Gunn, coloboma of disc, .... 83

„ Crick dots, . . 27, 67, 199 ; iv. 9, 10

,, macular reflex, . . . . 66

,, star-figure at macula, . . .136

,, thickened arteries in albuminuria, . 139

167,

pro-

Habershon, hereditary optic atrophy, .

Haemorrhage in albuminuric retinitis, .

,, anaemia,

,, glaucoma, .

,, leukaemia, .

„ intraocular,

,, „ causing retinitis

liferans,

„ _ „ in young men, .

,, into sheath of optic nerve,

,, ,, glaucomatous cup,

„ ,, retina,

,, subhyaloid,

Haemorrhagic retinitis,

Hair-shadows on retina,

Haller, arterial circle of,

Halo round disc, glaucomatous, 156 ; xlvii. 105, 100, Ul7
„ ,, „ physiological, . 41 ; ii. 6 ; vi. 15

„ ,, macula, ..... 62

Harlan, new vessels in vitreous . . .166

Hartridge, haemorrhage into glaucoma cup, .

,, star-figure at macula, .

Hemianopsia, ......

Hess, coloboma, microscopic examination,
Hirschberg, embolism, ....

„ „ with microscopic ex-

amination, .

Hoffman, coloboma with entire iris,

Holder, fracture of optic foramen,

Hutchinson, recurrent haemorrhage in young
men, .....

„ retinitis pigmentosa, without

night-blindness,

„ Tay’s choroiditis,

,, (jun.), choroiditis after concussion

of eye,

„ ,, new vessels in vitreous,

Hyaline outgrowths from lamina vitrea,

,, ,, ,, optic disc, .

„ thickening of retinal vessels, 138, 160, 207
Hyaloid artery, . . . . . . 59

Hydrocephalus causing optic atrophy,

Hyperaemia of choroid,

,, of disc,

Hypermetropia, disc in,

,, retinal vessels in,

153
137

167

168
196
167

146
172
124
169

168 ; xxxv. 7s, 79

169 ; xxxix.88,g9
168; xxxv. 79

169

137

114

70
176

180

71
150

172

204

105

113

166

200

203

. 150

41, 92, 120
41
55

Jackson, Hughlings, normal vision in papillitis, 118
Jaeger, light-streak on vessels, ... 48

Jessop, subhyaloid haemorrhage, . . . 71

226

INDEX.

Keratitis punctata in choroiditis,
Kingdon, symmetrical changes- at macula,
Knapp, pigment streaks on fundus,

PAGE

101

191

211

Lamina cribrosa, ....

„ „ in congenital crescent,

„ „ glaucoma,

„ „ optic atrophy,

,, ,, physiological cupping,

„ fusca, .....

,, vitrea of choroid, . . .

„ ,, ,, outgrowths from

Lang and Barrett, cilio-retinal vessels,
Lawford, retinal vessels all emerging at
margin of disc,

„ vascular loop on disc, .

Lead poisoning as cause of papillitis,

“ Leaf -like” choroiditis, . ' .

Leber, hereditary optic atrophy, .

„ rheumatic choroiditis, * .

Leuksemic retinitis, .

157

154

200

Light fundi,

Light-streak on vessels,

Limiting membranes of retina,

Little, W. S., vessel projecting into vitreous,
Locomotor ataxy causing optic atrophy,
Loops made by vessels on disc, .

Loring, chorio-capillaris, effect of,

,, light-streak on vessels, .

,, physiological cup, .

Lymph sheaths of choroidal vessels,

,, ,, retinal vessels,

Lymphoid deposits in leukaemia,

51
51
130
105
153
111
195 ; xxxiii.

■■ -hi.::

47
20
58
151
51, 53
17

196

Mackenzie, S., anaemia causing haemorrhage, 167
,, tortuosity of retinal vessels, 56

,, tubercle of choroid, . . 103

Macula, anatomy of, . . . . . 64

„ colloid change at, . . . . 202

„ ophthalmoscopic appearance of, 65; ii. 4, 6, 6;

iii. 7, &c.

„ reflexes at, . . . 62, 65, 66

„ stellate figure at, 135; xxxv. y8 ; xxxvii. 84
,, „ of unusual character, 135;

xxxviii M, 86

,, symmetrical changes at, in infants, 190
„ vessels of, . . . . 67

Malaria causing papillitis, . . . .124

Manz, opaque nerve fibres, microscopical ex-
amination, . . . . . 73

„ retinitis proliferans, . . . . 144

Margin of disc, ...... 40

Masselon, infiltration vitreuse de la retine, . 20 1

,, subhyaloid haemorrhage, . . 170

Measles causing papillitis, . . . 124, 129

Medullary sheaths of nerve fibres, . . 28

Meningitis causing papillitis, . . 124, 128

“ Metallic ” dots tin fundus,

Meyer, retinal vessels in syphilis, ' .
Michel, thrombosis of vena centralis, *.
Miley, prognosis in albuminuric retinitis,
Moles pigmented on retina,

Mooren, retinitis punctata albescens, .
Morton, S., choroido-retinal sclerosis, .

„ subhyaloid haemorrhage, .
Mules, perivasculitis,

„ vessels in albuminuric retinitis,

„ • white clot in retinal vessel,
Muller’s fibres, .....

Myopia, .

,, choroiditis in,

„ cicatricial lines in,

,, crescent in, .

,, detached retina in,

97 ; xxiii
. 97 ; xxiii."

PAGE

27, 199
162
187
140
201
201
108
171
162
162
182
20
97

53’ 54’ 55

143

215

29, 128
123, 128 •

Nerve-sheaths, ■ .

„ distension of,

,, incision of, . . . . 123*

Nettleship, central senile choroiditis, . . 102

„ dropping of fluid from nose with

papillitis, . . . . 129

,, embolism, microscopic examination, 180
„ new vessels in vitreous, . . 165

,, parallel ridges on fundus after

papillitis, . . . .134

,, tortuous vessels, ... 56

,, white dots and pigment changes

with night-blindness, . . 200

Neuritis (see Optic Neuritis), . . .114

Nieden, hyaline proliferations on disc, . 203

Night-blindness in choroiditis, . . . 99

,, choroido-retinal sclerosis, 108

„ retinitis pigmentosa, . 204

„ with white dots and pigment

changes, . . . 200

Nordensen, detachment of retina, . . 214

Norris, new vessels in vitreous, . . .164

Nose, escape of clear fluid from, in papillitis, 129
Nuclear layers of retina, . . . . 20

CEdema of choroid, . . . . .134

„ ,, optic nerve in papillitis, . . 122

„ „ retina, . . . . 99 ; xxv. 5S

Oeller, leuktemic retinitis, . . . .197

Ogilvie, hereditary optic atrophy, . . 153

Opaque nerve fibres, 72, 74 ; xii. 34, 35 ; xiii. 36, 3T ;

xiv.

„ ,, microscopic examination,

Ophthalmoscopic image, enlargement of,
Optic atrophy, ......

„ ,, after embolism,

injury, .
neuritis,

3S> 39

73
4
147
. 176

. 148

147 ; xxxii. Tl, 72;

XXXVIII.

INDEX.

227

Optic atrophy, hereditary, .
,, ,, in acromegaly,

disseminated sclerosis,

glaucoma.

TAGE

153
151
151
155

150

151
147
155

29, 114
150

„ ,, hydrocephalus,

,, ,, locomotor ataxy,

„ post-neuritic,

,, secondary to fundus affections,
chiasma, .....

„ pressure on,
disc, anatomy,

„ atrophy, ....

,, inflammation of,

„ ophthalmoscopic appearance of,

,, oval shape of, . . ».

„ unusual colour of, 38, 43, 74, ?7 ; v.

15 > vi*h 22 > 36> 37

foramen, fracture through, . . 150

nerve, anatomy, - . . 28

,, oedema of, . . _ .122

,, retro-bulbar affections of, 114, 115, 127
„ sheaths of,. . . . 29, 128

,, tumours of, . . . 124

,, vessels of, . . . . 31

,, wounds of, . . .122

neuritis, 114; xxxi. 66, 67, 6g,_69 ; xxxii.. 70;

xxxiii. u, ; xxxvi.

28
147
114
32
45
12> lli

from general causes,

,, intracranial causes,
,, orbital causes,
normal vision in, .
results of,
retro-bulbar, .
subsidence, . . I

symptoms of,

,, vesicle,

Orbit, cellulitis of,

„ periostitis,

„ tumours of,

,, wounds of,

Orbital veins, phlebitis of, .
Oval disc, ....

81
129
127
125
118
131
115, 127
31 ; xxxi. 66
118
68
124
124
124
124
188
45

Papillitis ( see Optic Neuritis),

Parent, astigmatic disc by indirect method,
Peltesohn, coloboma of disc,

Periphery of fundus, ophthalmoscopic appear-

114

ance of,

. 13, 17, 18

Perivasculitis, . . . .

161 ; xl. 90, 91

Phlebitis of cavernous sinus,

. 187

,, orbital veins, .

188

Physiological cup,

34 ; i. 2> 3)

Pigment dots in choroiditis,

„ ,, on retina,

. 18 ; x. 2g, 20

,, epithelium, .

„ in rupture of choroid, .

113

„ on disc,

• V< 11’ 13

Pigment moles on retina.

PAGE

ring round-disc, . . 44 ; i.j ; ii. 6, &c.

stippling, 16

,, streaks on fundus, . . . 210

Pigmentary retinitis (see Retinitis Pigmentosa), 204
PI ange, pigment streaks on fundus, . . 211

Plastic choroiditis, ..... 90

,, retinitis, . . . . .142

Popp, embolism, . . . . .176

„ ,, with microscopic examina-
tion, . . . .180

Porus opticus, ...... 33

Post-neuritic atrophy, 1 47 ; xxxii. 71, 72 ; xxxviii. 87
Posterior staphyloma, . . . 97 ; xxiii. 53

„ synechise in choroiditis, . . 101

Power, semicircular haemorrhage of macula, . 71

Puerperal septicaemia, suppurative choroiditis in, 90
Pulsation in retinal vessels, . ... 59

Punctate conditions of the fundus, 1 99 ; iv. 9, 10 ;
* xi.

Purkinje’s figures,

Pyaemia causing choroiditis,

,, „ papillitis, .

30, 31 ; xxxm. 75 ; xxxv. 78
. ' . ' 24

90
124

Randall, cilio-retinal vessels, ... 52

,, coloboma of disc, . . . . . 82

Recklinghausen, opaque nerve fibres, . . 73

Recurrent haemorrhage in young men, . 172

Reflex appearances of fundus, . . 41, 65

„ „ ,, concentric retinal

striation, . 25

,, ,, halo round disc, 41; ii.6;vi.15

,, ,, ,, macular reflexes, 65

,, ,, „ retinal radial striation, 25

,, „ „ shot-silk or watered

silk appearance, 25

Relapsing choroiditis with retinal oedema, . 99

Retina, anatomy, . . . . . 19

,, atrophy of, . . .115; xxxviii. 62

„ detachment of, 213 ; xlvi. 100, 101, 102, 103
„ „ in choroiditis, . . 101

,, ,, in intraocular growth, 217

„ „ in myopia, . . 215

„ parallel ridging of, . . 134; xxxii. 7o

„ reflex from, . . . . 25 ; ii. 4, 5, 6

,, vessels of (see Blood Vessels), . 36, 48, 49

Retinal haemorrhage (see Haemorrhage), . 168

Retinitis, . . . . . . .133

n I Kn rmnnuin 1 ‘17 • vvviii • v v vim

' S2> 84

albuminuric, 137 ; xxx\i. g0; xxxvii.

broken veins in, 138, 160 ;

xxxvi.

circinata,

diabetic,

haemorrhagic,

leukaemic,

pigmentosa, 204 ; xlii.
,, senilis,

80 5

142

. 141

1 68 ; xxxv. 79
195 ; xxxiii. 74
. ; xliii. 96 ; xliv. 97

. 106

228

INDEX.

PAGE

Retinitis pigmentosa, secondary to choroiditis, 99 ;

xix.

„ prognosis m,

,, proliferans,

Retro-bulbar neuritis,
Rheumatic choroiditis,
Rupture of choroid, .

,, „ equatorial,

111 ; xxx.

139

144

115

111

64’ 65

112

Sachsalber, hyaline proliferations on disc, . 203

Schafer and Golding Bird, anatomy of fovea, G4

Schnabel and Sachs, cilio retinal vessels, . 51

,, ,, embolism, . . .180

Schneller, light-streak on vessels, . . 48

Schultze, state of the blood in a case of

retinitis proliferans, . . . .183

Schwann, white matter of, . . . . 28

Schweigger, embolism with microscopical ex-
amination, . . . . . .180

Schweinitz de, colloid change at macula, . 202

Scleral ring, . . . . . 43 ; v. 13

„ in glaucoma, . 156 ; xlvii. 105, 106, 10T

Sclerosis, choroido-retinal, . . . .106

,, disseminated, . . . . 151

„ of walls of retinal vessels (see Blood

Vessels), . . . 161 ; xl. 90, 91

Sclerotic, 11

Scurvy as a cause of papillitis, . . . 124

„ „ retinal haemorrhage, . 167

Semicircular haemorrhages, . . 169;xxxix. 88

Senile choroiditis, . . . 98, 102 ; xxiv. 56

Serous choroiditis, ..... 89

Sheaths of optic nerve, . . . 29, 128

Sichel, embolism, microscopic examination, . 100

Siegrist, rupture of ciliary arteries, . . 113

Simple atrophy, 149

,, glaucoma, . . . . .155

Smith, Priestley, embolism and thrombosis

of retinal arteries, . 178

„ , embolism, microscopic

examination,

180

Spicer, retinal vessels in inherited syphilis, . 160

Stellate figure at macula (see Macula), . 135

Stephenson, coloboma of disc, partial, . 83

,, concentric retinal striation, . 25

„ measles causing papillitis, . 129

,, pigment dots, . . . . 19

,, ,, streaks, . . . 211

,, retinal veins, unusual course, . 54

Stilling, canal of, ... 59, 75

Story, light-streak on vessels, . . . 48

Story and Benson, aneurisms on retinal arteries, 162
Syphilis and choroiditis, . . . .109

,, choroido retinal sclerosis, . . 106

„ disease of retinal vessels, . 160,162

,, papillitis, . . . . .125

Symmetrical changes at macula in infants, .
Sympathetic ophthalmitis, hypersemia of
disc in, ......

190

Tabes dorsalis as cause of atrophy,
Talko, coloboma with entire iris,
Tay’s choroiditis,

„ symmetrical changes at macula,
Theobald, new vessels in vitreous,
Thrombosis of cavernous sinus, .

„ of central artery,

„ „ vein,

of retinal veins,

151
71

105
190
165
187
174, 179

. 187 ; xxxiv. 76, n
189 ; xxxvii. 83

Tortuosity of retinal vessels, 51, 55 ; vii. 18, 19 ; xxi.
Tubercle as a cause of choroiditis, 99, 103, 110
Tumour, intracranial, . . . . .124

„ intraocular, . . . . .217

„ of optic nerve, . . . .124

„ of orbit, . . . . .124

Ulrich, intracranial growths, autopsies, . 122

,, disseminated sclerosis, as cause of

atrophy, . . . . .151

Usher, opaque nerve fibres, microscopic

examination, . . . . . 73

Vascular system of retina, . . . .158

Veins, bifurcation of, . . . . 54

,, choroidal, . . . . . 15

,, retinal, thrombosis of, . 189; xxxvii. 83

„ „ tortuosity, 51, 55 ; vii. 18, 19 ; xxi. 48

Vense vorticosse, . . . . . 15

Vitreous, bands in, . . . .145

, , dust-like opacities in, . . . 118

„ new vessels in, . . . 163; xl. 91

„ opacities in choroiditis, . . 100

„ undue fluidity of, . . . 101

Wadsworth, symmetrical changes at macula, 194
Wagenmann, opaque nerve fibres disappearing

in atrophy, . . . . . . 75

Walser, pigment streaks on fundus, . . 211

Wedl and Bock, colloid change in pigment

layer, ....... 202

Wolf, W., embolism with microscopic

examination, . . .180

„ thrombosis of vena centralis, . 187

Wood, White, embolism, recovery during

examination, . . . . . .181

Wounds of globe causing papillitis, . . 124

,, „ ,, hypersemia of choroid, 91

,, optic nerve, . . . 124, 150

,, orbit, 125

Yellow spot ( see Macula),

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Plates from Original Drawings, price 25s.

DISEASES OF THE EYE : a Practical Treatise for Students of Ophthalmology. By GEORGE A.

BERRY, M.B., F.R.C.S.Ed., Ophthalmic Surgeon, Edinburgh Royal Infirmary; Lecturer on Ophthalmology, Royal
College of Surgeons, Edinburgh. ' [ Pentland’s Medical Series.— Vol. II.

Second Edition, Revised and Enlarged, 8vo, cloth, pp. xvi., 682, with Coloured Illustrations from Original Drawings, price 25s.

DISEASES OF THE THROAT, NOSE AND EAR. By P. M‘BRIDE, M.D., F.R.C.P.Ed., Lecturer on the

Diseases of the Ear and Throat, Edinburgh School of Medicine ; Aural Surgeon and Laryngologist, Royal Infirmary,
Edinburgh ; Surgeon, Edinburgh Ear and Throat Dispensary. [Pentland’s Medical Scries. — Vol. III.

8vo, cloth", pp. xvi., 508, price 16s.

TEXT-BOOK OF ABDOMINAL SURGERY : a Clinical Manual for Practitioners and Students. By

SKENE KEITH, F.R.C.S.Ed., assisted by GEORGE E. KEITH. M.B. [Pentland’s Medical Series.— Vol. IV.

8vo, cloth, pp. xx., 506, Illustrated with numerous Engravings throughout the text, price 16s.

FUNCTIONAL AND ORGANIC DISEASES OF THE STOMACH. By SIDNEY MARTIN, M.D.,

F.R.S., F.R.C.P., Assistant Physician and Assistant Professor of Clinical Medicine at University College Hospital;
Assistant Physician to the Hospital for Consumption and Diseases of the Chest, Brompton.

[Pentland’s Medical Series. — Vol. Y.

Third Enlarged and thoroughly Revised Edition, 8vo, cloth, pp. xx., 652, Illustrated with 195 Coloured Plates

from Original Drawings, price 25s.

PRACTICAL PATHOLOGY : a Manual for Students and Practitioners. By GERMAN SIMS

WOODHEAD, M.D., F.R.C.P.Ed., Director of the Laboratories of the Royal College of Physicians (London) and
Surgeons (England).

Second Edition, thoroughly Revised, Two Volumes, crown 8vo, cloth, Illustrated with numerous Wood Engravings. Vol. I. —
Upper Limb, Lower Limb, Abdomen. Vol. II. — Thorax, Head and Neck. Price per Volume, 12s. 6d.

MANUAL OF PRACTICAL ANATOMY. By D. J. CUNNINGHAM, M.D., Professor of Anatomy and

Surgery, Trinity College, Dublin. [Pentland’s Students’ Manuals.

8vo, cloth, pp. xvi., 374, with 63 Engravings in the text, price 14s. nett.

TUBERCULOUS DISEASE OF THE BONES AND JOINTS. By W. WATSON CHEYNE, M.B.,

F.R.S., Professor of Surgery, King’s College, London.

8 vo, cloth, pp. xvi., 240, with 22 pp. of Plates and Figures throughout the text, price 12s. 6d. nett.

ECTOPIC PREGNANCY : its Etiology, Classification, Embryology, Diagnosis, and Treatment. By

J. CLARENCE WEBSTER, M.D., F.R.C.P.Ed., Assistant to the Professor of Midwifery and Diseases of Women and
Children in the University of Edinburgh.

Large 8vo, cloth, pp. xxviii., 772, Illustrated with 404 Engravings, price 31s. 6d.

THE PARASITES OF MAN, and the Diseases which proceed from them. A Text-Book for Students and

PRACTITIONERS. By RUDOLF LEUCKART, Professor of Zoology and Comparative Anatomy in the
University of Leipsic. Translated from the German, with the Co-operation of the Author, by William E. Hoyle,
M.A. (Oxen), M.R.C.S., F.R.S.E., Curator of the Museums, Owens College, Manchester. Natural History of
Parasites in general — Systematic Account of the Parasites infesting Man — Protozoa — Cestoda.

Two vols., large 8vo, cloth, pp. xvi., 1000, Illustrated with Maps and Charts, price 31s. 6d.

GEOGRAPHICAL PATHOLOGY : an Inquiry into the Geographical Distribution of Infective and

CLIMATIC DISEASES. By ANDREW DAVIDSON, M.D., F.R.C.P.Ed., late Visiting and Superintending
Surgeon, Civil Hospital ; Professor of Chemistry, Royal College, Mauritius.

Oblong 4to, Cloth, in a series of 27 Coloured Plates from Original Drawings, with Descriptive Letterpress,
and 27 Engravings throughout the Text. Price 50s. nett.

ILLUSTRATIONS OF THE NERVE TRACTS in the Mid and Hind Brain, and the Cranial Nerves

ARISING THEREFROM. By ALEXANDER BRUCE, M.D., F.R.C.P.Ed., Lecturer on Pathology in the
School of Medicine, Edinburgh ; Assistant Physician (formerly Pathologist), Edinburgh Royal Infirmary ; Pathologist
to the Royal Hospital for Sick Children.

Volumes I.-III., 8vo, cloth, gilt tops, pp. 500 or thereby each. Illustrated with Full Page Plates, many in Colours,
and numerous Engravings throughout the text, price 25s. per volume.

THE JOURNAL OF PATHOLOGY AND BACTERIOLOGY. Edited with the Collaboration of Distinguished
British and Foreign Pathologists, by GERMAN SIMS WOODHEAD, M.D., Edin., Director of the Laboratories of
the Royal Colleges of Physicians (London) and Surgeons (England).

One Volume, royal 8vo, cloth, pp. xviii., 1014, Illustrated, price 31s. 6d,

THE HYGIENE AND DISEASES OF WARM CLIMATES: in a Series of Articles by Eminent

AUTHORITIES. Edited by ANDREW DAVIDSON, M.D., F.R.C.P.Ed., late Visiting and Superintending
Surgeon, Civil Hospital ; Professor of Chemistry, Royal College, Mauritius ; Author of “Geographical Pathology.”

YOUNG J. PENTLAND,

Edinburgh: ii Teviot Place. London: 38 West Smithfield, E.C.

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